Moderate-intensity Static Magnetic Field Research Articles

Acetaminophen overdose-induced acute liver injury can be alleviated by static magnetic field.

Acetaminophen (APAP), the most frequently used mild analgesic and antipyretic drug worldwide, is implicated in causing 46% of all acute liver failures in the USA and between 40% and 70% in Europe. The predominant pharmacological intervention approved for mitigating such overdose is the antioxidant N-acetylcysteine (NAC); however, its efficacy is limited in cases of advanced liver injury or when administered at a late stage. In the current study, we discovered that treatment with a moderate intensity static magnetic field (SMF) notably reduced the mortality rate in mice subjected to high-dose APAP from 40% to 0%, proving effective at both the initial liver injury stage and the subsequent recovery stage. During the early phase of liver injury, SMF markedly reduced APAP-induced oxidative stress, free radicals, and liver damage, resulting in a reduction in multiple oxidative stress markers and an increase in the antioxidant glutathione (GSH). During the later stage of liver recovery, application of vertically downward SMF increased DNA synthesis and hepatocyte proliferation. Moreover, the combination of NAC and SMF significantly mitigated liver damage induced by high-dose APAP and increased liver recovery, even 24 h post overdose, when the effectiveness of NAC alone substantially declines. Overall, this study provides a non-invasive non-pharmaceutical tool that offers dual benefits in the injury and repair stages following APAP overdose. Of note, this tool can work as an alternative to or in combination with NAC to prevent or minimize liver damage induced by APAP, and potentially other toxic overdoses.

Exposure to a static magnetic field attenuates hepatic damage and function abnormality in obese and diabetic mice

Static magnetic fields (SMFs) exhibit significant effect on health care. However, the effect of SMF on hepatic metabolism and function in obesity and diabetes are still unknown. Liver is not only the main site for glucolipid metabolism but also the core part for iron metabolism regulation. Dysregulations of iron metabolism and redox status are risk factors for the development of hepatic injury and affect glucolipid metabolism in obesity and diabetes. Mice of HFD-induced obesity and HFD/streptozocin-induced diabetes were exposed to a moderate-intensity SMF (0.4–0.7 T, direction: upward, 4 h/day, 8 weeks). Results showed that SMF attenuated hepatic damage by decreasing inflammation and fibrosis in obese and diabetic mice. SMF had no effects on improving glucose/insulin tolerance but regulated proteins (GLUT1 and GLUT4) and genes (G6pc, Pdk4, Gys2 and Pkl) participating in glucose metabolism with phosphorylation of Akt/AMPK/GSK3β. SMF also reduced lipid droplets accumulation through decreasing Plin2 and Plin5 and regulated lipid metabolism with elevated hepatic expressions of PPARγ and C/EBPα in obese mice. In addition, SMF decreased hepatic iron deposition with lower FTH1 expression and modulated systematic iron homeostasis via BMP6-mediated regulation of hepcidin. Moreover, SMF balanced hepatic redox status with regulation on mitochondrial function and MAPKs/Nrf2/HO-1 pathway. Finally, we found that SMF activated hepatic autophagy and enhanced lipophagy by upregulating PNPLA2 expression in obese and diabetic mice. Our results demonstrated that SMF significantly ameliorated the development of hepatic injury in obese and diabetic mice by inhibiting inflammatory level, improving glycolipid metabolism, regulating iron metabolism, balancing redox level and activating autophagy.

The Effect of a Static Magnetic Field on microRNA in Relation to the Regulation of the Nrf2 Signaling Pathway in a Fibroblast Cell Line That Had Been Treated with Fluoride Ions

Many physical and chemical factors can influence the Nrf2 signaling pathway, and its deregulation has been associated with various disease states. Nrf2 and Keap1 molecules are key elements that regulate the response under cell stress conditions. Hence, the aim of the research was to assess the impact of a static magnetic field that was generated by permanent magnets on the transcriptional activity of the NFE2L2 and KEAP1 genes in a human dermal fibroblast cell line that had been cultured with fluoride ions and in an environment without them. Additionally, our research aimed to answer the question of whether the regulatory RNA molecules—miRNAs—are involved in these effects. Experiments were performed on an NHDF cell line that had been treated with fluoride ions, along with simultaneous exposure to a moderate-intensity static magnetic field. The RT-qPCR method was used to determine the mRNA level of the NFE2L2 and KEAP1 genes and the miRNA level of miR-28-3p, miR-29b-1-5p, miR-141-3p and miR-365a-3p. Our results indicate that fluoride ions influence the Nrf2 signaling pathway and that miRNAs are involved in regulating it. Moreover, the static magnetic field had a beneficial effect on the cells with fluoride-induced oxidative stress due to stimulating the antioxidant defense.

Moderate intensity of static magnetic fields can alter the avoidance behavior and fat storage of Caenorhabditis elegans via serotonin.

Man-made static magnetic fields (SMFs) widely exist in human life as a physical environmental factor.However, the biological responses to moderate SMFs exposure and their underlying mechanisms are largely unknown. The present study was focused on exploring the nervous responses to moderate-intensity SMFs at 0.5T and 1T in Caenorhabditis elegans (C. elegans). We found that SMFs at either 0.5T or 1T had no statistically significant effects on the locomotor behaviors, while the 1T magnetic field increased pharyngeal pumping. The avoidance behavior of the pathogenic Pseudomonas aeruginosa was greatly decreased in either 0.5T or 1T SMFs exposed nematodes, and the learning index was reducede from 0.52 ± 0.11 to 0.23 ± 0.17 and 0.16 ± 0.11, respectively. The total serotonin level was increased by 17.08% and 16.45% with the treatment of 0.5T and 1T SMF, compared to the control group; however, there were minimal effects of SMFs on other three neurotransmitters including choline, γ-aminobutyric acid (GABA), dopamine. RT-qPCR was used to further investigate the expression of serotonin-related genes, including rate-limiting enzymes, transcription factors and transport receptors. The expression levels of tph-1 and unc-86 genes were increased by SMF exposure, while those of ocr-2, osm-9, ser-1 and mod-1 genes were decreased. With the staining of lipid in either wild-type N2 or tph-1 mutants, we found that 0.5T and 1T SMFs decreased fat storage in C. elegans via serotonin pathway. Our study demonstrated that moderate-intensity SMFs induced neurobehavioral disorder and the reduction of fat storage by disturbing the secretion of serotonin in C. elegans, which provided new insights into elucidating nervous responses of C. elegans to moderate-intensity SMFs.

Static Magnetic Fields Enhance the Chondrogenesis of Mandibular Bone Marrow Mesenchymal Stem Cells in Coculture Systems.

Objectives Combining the advantages of static magnetic fields (SMF) and coculture systems, we investigated the effect of moderate-intensity SMF on the chondrogenesis and proliferation of mandibular bone marrow mesenchymal stem cells (MBMSCs) in the MBMSC/mandibular condylar chondrocyte (MCC) coculture system. The main aim of the present study was to provide an experimental basis for obtaining better cartilage tissue engineering seed cells for the effective repair of condylar cartilage defects in clinical practice. Methods MBMSCs and MCCs were isolated from SD (Sprague Dawley) rats. Flow cytometry, three-lineage differentiation, colony-forming assays, immunocytochemistry, and toluidine blue staining were used for the identification of MBMSCs and MCCs. MBMSCs and MCCs were seeded into the lower and upper Transwell chambers, respectively, at a ratio of 1 : 2, and exposed to a 280 mT SMF. MBMSCs were harvested after 3, 7, or 14 days for analysis. CCK-8 was used to detect cell proliferation, Alcian blue staining was utilized to evaluate glycosaminoglycan (GAG), and western blotting and real-time quantitative polymerase chain reaction (RT-qPCR) detected protein and gene expression levels of SOX9, Col2A1 (Collagen Type II Alpha 1), and Aggrecan (ACAN). Results The proliferation of MBMSCs was significantly enhanced in the experimental group with MBMSCs cocultured with MCCs under SMF stimulation relative to controls (P < 0.05). GAG content was increased, and SOX9, Col2A1, and ACAN were also increased at the mRNA and protein levels (P < 0.05). Conclusions Moderate-intensity SMF improved the chondrogenesis and proliferation of MBMSCs in the coculture system, and it might be a promising approach to repair condylar cartilage defects in the clinical setting.

Static Magnetic Field (0.2-0.4 T) Stimulates the Self-Renewal Ability of Osteosarcoma Stem Cells Through Autophagic Degradation of Ferritin.

Static magnetic field (SMF) can alter cell fate decisions in many ways. However, the effects of SMF on cancer stem cells (CSCs) are little-known. In this particular study, we evaluate the biological effect of moderate-intensity SMF on osteosarcoma stem cells (OSCs) and try to clarify the underlying mechanisms of action. First, we demonstrated that prolonged exposure to SMF induced the proliferation and tumorsphere formation in K7M2 and MG63 OSCs. Moreover, SMF promoted the release of ferrous iron (Fe2+ ) and provoked reactive oxygen species (ROS) in OSCs. Interestingly, SMF evidently triggered the autophagic degradation of ferritin, which is characterized by the activation of microtubule-associated protein 1 light chain 3 (LC3) and nuclear receptor co-activator 4 (NCOA4), and downregulation of ferritin heavy chain 1 (FTH1) in OSCs. Particularly, the colony-forming ability of K7M2 OSCs promoted by SMF was obviously abolished by using a small interfering RNA (siRNA) against NCOA4. Finally, treatment of the tumor-bearing mice with SMF did not affect the tumor volume or tumor mass, nor pulmonary metastasis of K7M2 OSCs, but the SMF-treated K7M2 OSCs caused a preference of pulmonary metastasis in a mouse model, which suggested that SMF might induce the metastatic characteristic of OSCs. Consequently, this paper demonstrates for the first time that the cumulative SMF exposure promoted the self-renewal ability of OSCs via autophagic degradation of ferritin, implying that ferritinophagy may be a potential molecular target for cancer. © 2021 Bioelectromagnetics Society.

Moderate Static Magnetic Fields Prevent Bone Architectural Deterioration and Strength Reduction in Ovariectomized Mice

Substantial studies have revealed the capacity of moderate-intensity static magnetic fields (SMFs) on promoting osteogenesis and inhibiting bone resorption. However, it is unknown whether moderate SMF can resist the deterioration of bone microarchitecture and strength induced by the reduction of estrogen in animal model for postmenopausal osteoporosis. Herein, the efficiency of moderate SMF of 0.2~0.4 T and SMF of 0.6 T on bone mineral density (BMD) and bone mineral content (BMC), bone microarchitecture, bone strength, and histological bone turnover was systematically investigated in ovariectomized (OVX) mice. OVX mice and sham mice were subjected to SMF exposure continuously for four weeks. Dual-energy X-ray absorptiometry (DEXA) data showed SMF prevented the reduction of BMD and BMC in OVX mice. Micro-computed tomography (Micro-CT) results revealed that SMF ameliorated the deterioration of trabecular and cortical bone microarchitecture. Three-point bending test showed that SMF mitigated OVX-induced reduction in femoral mechanical properties, including stiffness, ultimate stress, and elasticity modulus. Moreover, bone histochemical analysis demonstrated that SMF decreased osteoclast formation in cancellous bone and cortical bone, while SMF increased osteoblast formation in trabecular bone. Together, these results demonstrate that moderate SMF alleviated menopause-induced bone loss effectively, and imply that moderate SMF might become a potential biophysical treatment modality for postmenopausal osteoporosis.

Static magnetic field induces abnormality of glucose metabolism in rats’ brain and results in anxiety-like behavior

In this study, fifty-four male Wistar rats were randomly divided into four groups according to the static magnetic field (SMF) intensity, namely, control, low-intensity, moderate-intensity, and high-intensity groups. The rats' whole body was exposed to a superconducting magnet exposure source. The exposure SMF intensity for the low-intensity, moderate-intensity, and high-intensity groups was 50 m T, 100 m T, and 200 m T, respectively, and the exposure time was 1 h/day for consecutive 15 days. After different exposure times, glucose metabolism in rats' brain was evaluated by micro-positron emission tomography (micro-PET), and the expression of hexokinase 1(HK1) and 6-phosphate fructokinase-1(PFK1) was detected by western blot. The exploration and locomotion abilities of the rats were evaluated by conducting open field test (OFT). Furthermore, pathological changes of rats' brain were observed under a microscope by using hematoxylin–eosin staining. PET results showed that moderate-intensity SMFs could cause fluctuant changes in glucose metabolism in rats' brain and the abnormalities were SMF intensity dependent. The expression of the two rate-limiting enzymes HK1 and PFK1 in glucose metabolism in brain significantly decreased after SMF exposure. The OFT showed that the total distance, surrounding distance, activity time, and climbing and standing times significantly decreased after SMF exposure. The main pathological changes in the brain were pyknosis, edema of neurons, and slight widening of the perivascular space, which occurred after 15 times of exposure. This study indicated that SMF exposure could lead to abnormal glucose metabolism in the brain and might result in anxiety-like behaviors.

Protective Effects of Moderate Intensity Static Magnetic Fields on Diabetic Mice.

The purpose of this study was to investigate the effects of moderate-intensity static magnetic field (SMF) on diabetic mice. We studied the effects of SMF on blood glucose of normal mice by starch tolerance and glucose tolerance tests. Then, we evaluated the effects of SMF on blood glucose of diabetic mice by establishing alloxan-induced type 1 diabetic mice and high-fat diet + streptozotocin (STZ)-induced type 2 diabetic mice. The results showed that different magnetic field intensities and blank control did not affect the blood glucose of normal mice. After starch and glucose administration, different magnetic fields could improve the glucose tolerance of normal mice, and this was obvious in the600 mT group. In the experiment of type 1 diabetic mice induced by alloxan, the results showed that different magnetic field intensities could improve the starch tolerance of mice, and that in the 400 mT group was obvious. In the experiment of type 2 diabetic mice induced by a high-fat diet + STZ, the 400 mT group could reduce food intake and water consumption in the later period. The 600 mT group could improve the starch tolerance of mice. The 400 and 600 mT groups could reduce fasting blood glucose. At the same time, total cholesterol and triglyceride decreased in different magnetic field intensities, and the 600 mT group could significantly increase the serum insulin content of mice. In summary, the results of this study suggest that SMF has a protective role in diabetic mice. Bioelectromagnetics. © 2020 Bioelectromagnetics Society.

Anti-apoptotic effect of a static magnetic field in human cells that had been treated with sodium fluoride

Static magnetic field (SMF) is widely used in industry, in consumer devices and diagnostic medical equipment, hence the widespread exposure to SMF in the natural environment and in people occupationally exposed to it. In environment and in some workplaces, there is a risk of exposure also to various chemicals. Environmental factors can affect the cellular processes which can be the cause of the development of various pathological conditions. Therefore, the aim of this study was to assess the effect of SMF on the expression of the apoptosis-related genes in human fibroblast cultures that had been co-treated with fluoride ions. The control and NaF-treated cells were subjected to the influence of SMF with a moderate induction. The flow-cytometric analysis showed that the fluoride ions reduced the number of viable cells and induced early apoptosis. However, exposure to the SMF reduced the number of dead cells that had been treated with fluoride ions. Moreover, specific genes that were involved in apoptosis exhibited a differential expression in the NaF-treated cells and exposure to the SMF yielded a modulation of their transcriptional activity. Our results suggest some beneficial properties of using a moderate-intensity static magnetic field to reduce the adverse effects of fluoride.

Moderate Intensity Static Magnetic Fields Prevent Thrombus Formation in Rats and Mice.

We established three types of thrombosis models to explore the effects of the static magnetic field (SMF) on thrombosis in rats and mice with three different MF intensities. In the carrageenan-induced thrombosis model in rats, the SMF treatments reduced the black tail length of rats, extracorporeal thrombus, and the mass of wet and dry thrombus, and improved the coagulation index value. In FeCl3 -induced arterial thrombosis model in rats, the SMF treatment showed some anti-thrombotic effects. More specifically, the SMF treatment affected rodent blood pressure, plasma plasminogen activator inhibitor, tissue-type plasminogen activator, thrombus mass, and thrombus protein content. In the adrenaline-induced thrombosis model in mice, the SMF treatment had certain effects on the diameter and blood flow velocity of mouse auricle microcirculation in fine veins and arteries. Overall, the highest MF intensities we tested, 20-150 mT, showed a trend of anti-thrombotic effect, indicating that the moderate-intensity SMF might serve as a potential treatment for clot-related diseases in the future. Bioelectromagnetics. 2020;41:52-62 © 2019 Bioelectromagnetics Society.

Static Magnetic Field Induced Neural Stem/Progenitor Cell Early Differentiation and Promotes Maturation.

The potential impacts of magnetic field exposures on brain development have raised public concern. In the present study, we aimed to investigate the biophysical effects of moderate-intensity (0.5 T, Tesla) static magnetic field (SMF) on mice neural progenitor cells (mNPCs). Our results showed that the SMF exposure increased the number of neurosphere formation and enhanced proliferative activity in mNPCs. In addition, our flow cytometry data demonstrated that the proportions of S phase and G2/M phase mNPCs were remarkably increased following 5 days of SMF exposure. Moreover, the level of a mitotic regulatory protein, cyclin B, was upregulated after SMF exposure. Furthermore, the mNPCs exposed to SMF exhibited a significant increase in Sox2 expression. When mNPCs were induced to differentiation, our immunofluorescence assay revealed that the percentage of neurons (Tuj-1-positive cells) but not astrocyte (s100β-positive cells) was significantly higher and displayed morphological complexity in the SMF group. Finally, our electrophysiological results demonstrated the mNPC-derived neurons from the SMF group showing a significantly increased in input resistance, which indicated more functional maturation. Based on these findings, it appears reasonable to suggest that SMF exposure could affect normal neurogenesis and promote neural lineage differentiation as well as neuronal maturation.

The effect of simultaneous exposure of human fibroblasts to fluoride and moderate intensity static magnetic fields

Background: The combined effect of exposure to a static magnetic field (SMF) and potentially toxic agents is a crucial research area, mainly due to occupational and environmental exposure to these factors. The aim of this study was to evaluate the effect of the simultaneous exposure of human fibroblasts to fluoride and a SMF.Materials and methods: Control fibroblasts and fibroblasts that had been treated with fluoride were subjected to an SMF at a moderate induction (0.45, 0.55 and 0.65 T). The intracellular reactive oxygen species production, the concentration of malondialdehyde and the activities of superoxide dismutase and glutathione peroxidase were measured.Results: Our investigations revealed that a moderate SMF does not enhance the action of fluoride in inducing oxidative stress by generating free radicalsConclusions: A moderate SMF may be a factor that weakens the toxic action of fluoride, which is important for the health of individuals that are co-exposed to an SMF and fluoride ions (F−) from occupational and environmental sources.

Enhanced Biodecolorization Performance of Azo Dyes Under High-Salt Conditions by a Marine Microbial Community Exposed to Moderate-Intensity Static Magnetic Field

Abstract Effects of moderate-intensity static magnetic field (SMF) on biodecolorization of azo dyes by a marine microbial community (MMC) and halotolerance of the consortium were investigated. Perf...

Application of a static magnetic field as a complementary aid to healing in an in vitro wound model

Static magnetic field (SMF) has long been used as a therapeutic means, though its effects on the activity of cells and the mechanism(s) involved remain unknown. The purpose of this study is to determine the effect of a moderate-intensity SMF on the activity, growth and migration of mouse embryonic fibroblast (NIH 3T3), aiming to mimic wound healing and to study it in real time. A cell-free area (a scratch with a 200-500µm width) was formed in NIH 3T3 cultured cells and used as a wound model. The effects of a SMF (10, 50, 80 and 100mT) on the survival rate (MTT assay), integrity of cell membranes (lactate dehydrogenase (LDH) assay), the morphology of the cell (circularity, number and length of filopodia), cell orientation, and migration (speed, direction, rate) were studied as a function of the incubation time in a time-lapse manner. The exposure of cells to SMF at all intensities had no cytotoxic effect, as revealed by the MTT assay. The integrity of the membranes of the SMF-treated cells studied by the LDH assay test showed no effects. The structure of the membrane at the leading edge of the cells changed and showed several filopodia extended parallel to the field direction. The exposure to the SMF elongated the cells and decreased their circularity at SMF 10mT. The migration of the cells from one edge of the gap towards the other was affected by the applied SMF. The maximum and minimum effects were monitored at 80mT and 10mT, respectively. Analysis of cell migration revealed an average directness of 0.73, 0.66, 0.78, 0.78 and 0.69 under SMF 10, 50, 80, 100mT and control, respectively. The morphological and functional changes of the cells in the presence of SMF revealed particular effects on the membrane and cytoskeleton. Cells were affected by physicochemical changes caused by the applied SMF, though the extent of the incurred effects was not a linear function of the field intensity. This low cost, non-invasive approach can be used as a magneto-manipulative means to tailor a practical, independent or complementary means of manipulating the activities of cells and tissues for clinical purposes.

Effects of static magnetic fields on natural or magnetized mesenchymal stromal cells: Repercussions for magnetic targeting

The magnetic targeting (MT) technique improves delivery of mesenchymal stromal cells (MSCs) to target sites. However, the moderate-intensity static magnetic fields (SMF) used for MT may exert adverse effects on MSCs. Thus, we aimed to evaluate the effects of SMF on MSCs in vitro. Cells were initially magnetized using citrate-coated magnetite nanoparticles. Then, control and magnetized MSCs were transferred to an in vitro MT system and exposed to 0.3–0.45 Tesla SMFs. MSC viability, morphology, ultrastructure, proliferation rates, differentiation, and immunomodulation were evaluated after 24 and 48 hours of exposure. MSCs temporarily lost viability and exhibited ultrastructural changes after exposure to SMFs, regardless of magnetization. Moreover, exposure to SMF reduced magnetized MSC proliferation rates. Nevertheless, MSCs remained functional (i.e., capable of differentiating, secreting repair mediators, and modulating alveolar macrophage phenotype). Thus, the experimental protocol tested in this experiment can be applied in future in vivo MT studies.

Effects of moderate intensity static magnetic fields on osteoclastic differentiation in mouse bone marrow cells.

Although we recently demonstrated that static magnetic fields (SMFs) of 3, 15, and 50 mT stimulate osteoblastic differentiation, the effects of SMFs on osteoclastogenesis are still poorly understood. This study focused on the suppressive effects of SMFs on receptor activator of nuclear factor κB ligand (RANKL)-induced osteoclastogenesis and bone resorption. Direct SMFs inhibit RANKL-induced multinucleated osteoclast formation, tartrate-resistant acid phosphatase activity, and bone resorption in mouse bone marrow-derived macrophage cells. The conditioned medium from osteoblasts treated with SMFs also resulted in the inhibition of osteoclast differentiation as well as resorption. The RANKL-induced expression of osteoclast-specific transcription factors, such as c-Fos and NFATc1, was remarkably downregulated by SMF at 15 mT. In addition, SMF inhibited RANKL-activated Akt, glycogen synthase kinase 3β (GSK3β), extracellular signal-regulated kinase, c-jun N-terminal protein kinase, mitogen-activated protein kinase (MAPK), and nuclear factor-κB (NF-κB) formation. These findings indicate that SMF-mediated attenuation of RANKL-induced Akt, GSK3β, MAPK, and NF-κB pathways could contribute to the direct and indirect inhibition of osteoclast formation and bone resorption. Therefore, SMFs could be developed as a therapeutic agent against periprosthetic or peri-implant osteolysis. Additionally, these could be used against osteolytic diseases such as osteoporosis and rheumatoid arthritis. Bioelectromagnetics. 39:394-404, 2018. © 2018 Wiley Periodicals, Inc.

Moderate-intensity 4 mT static magnetic fields prevent bone architectural deterioration and strength reduction by stimulating bone formation in streptozotocin-treated diabetic rats

Type 1 diabetes mellitus (T1DM) has been associated with deterioration of bone microarchitecture and strength, resulting in increased fracture risk. Substantial studies have revealed the capacity of moderate-intensity static magnetic fields (SMF) on promoting osteoblastogenesis in vitro and stimulating bone growth and bone regeneration in vivo, whereas it is unknown whether SMF can resist T1DM-associated osteopenia/osteoporosis. We herein investigated the potential effects of whole-body SMF exposure with 4mT on bone loss in streptozotocin-induced T1DM rats. We found that SMF exposure for 16weeks inhibited architectural deterioration of trabecular bone and cortical bone and mechanical strength reduction in T1DM rats, as evidenced by the MicroCT and 3-point bending findings. Our serum biochemical, bone histomorphometric and PCR results revealed that SMF induced higher serum osteocalcin, mineral apposition rate and osteoblast number of trabecular bone, and higher skeletal osteocalcin, BMP2 and Runx2 gene expression in T1DM rats, whereas SMF showed no significant alteration in serum CTX, skeletal osteoclast number, or osteoclastogenesis-related RANKL-RANK signaling gene expression. Together, our findings suggest that moderate SMF prevented bone architectural deterioration and strength reduction by inhibiting the reduction of bone formation in T1DM rats, and indicate that SMF might become a promising biophysical countermeasure for T1DM-related osteopenia/osteoporosis.

Moderate intensity static magnetic fields affect mitotic spindles and increase the antitumor efficacy of 5-FU and Taxol

Microtubules are the fundamental components in mitotic spindle, which plays essential roles in cell division. It was well known that purified microtubules could be affected by static magnetic fields (SMFs) in vitro because of the diamagnetic anisotropy of tubulin. However, whether these effects lead to cell division defects was unknown. Here we find that 1T SMFs induce abnormal mitotic spindles and increase mitotic index. Synchronization experiments show that SMFs delay cell exit from mitosis and cause mitotic arrest. These mimic the cellular effects of a microtubule-targeting drug Paclitaxel (Taxol), which is frequently used in combination with 5-Fluorouracil (5-FU) and Cisplatin in cancer treatment. Using four different human cancer cell lines, HeLa, HCT116, CNE-2Z and MCF7, we find that SMFs increase the antitumor efficacy of 5-FU or 5-FU/Taxol, but not Cisplatin, which indicates that the SMF-induced combinational effects with chemodrugs are drug-specific. Our study not only reveals the effect of SMFs on microtubules to cause abnormal mitotic spindles and delay cells exit from mitosis, but also implies the potential applications of SMFs in combination with chemotherapy drugs 5-FU or 5-FU/Taxol, but not with Cisplatin in cancer treatment.

1 T moderate intensity static magnetic field affects Akt/mTOR pathway and increases the antitumor efficacy of mTOR inhibitors in CNE-2Z cells

Static magnetic field (SMF) has been known to affect cell proliferation in a cell-type-dependent manner, while the mechanism still remains unclear. We found that 1T moderate intensity SMF inhibits cell proliferation of nasopharyngeal carcinoma CNE-2Z cells and the Akt/mTOR signaling pathway, which is upregulated in many cancers. mTOR inhibitors are potential chemodrugs, but their clinical effects are limited by the feedback reactivation of other signaling components such as EGFR and Akt. We showed that 1T SMF increases the antitumor efficacy of mTOR inhibitor Torin 2. In addition, 1T SMF increases the inhibition efficiency on mTOR substrates phosphorylation and represses the mTOR inhibitor-induced feedback reactivation of EGFR and Akt. Our study not only demonstrates that mTOR/Akt pathway is one of the molecular targets of SMFs in cells, but also reveals the clinical potentials of combinations of mTOR inhibitors and SMFs in cancer treatment.