With the rise of magnetic therapy, biological effects of magnetic field have gotten more and more attention in recent years. Based on literatures both at home and abroad, this article summarized research status of biological effects of static magnetic field on whole level, tissue-organ level, cellular level and molecular level of living organisms. We found that conclusions and results of researches varied with different purposes and experiment methods, demonstrating that researches on dose-response relationship and safety of static magnetic field were necessary.

Objective To explore the magnetic properties of permanent magnet wafers commonly used in magnetotherapy to provide a basis for the scientific and rational use of sources of magnetism.Methods A magnetometer was used to measure the magnetic induction intensities of the N and S polar centers of eight groups of magnet wafers (axial magnetization) with nominal magnetic induction intensities of 6 mT, 10 mT, 20 mT, 30 mT, 60 mT,100 mT, 200 mT and 350 mT.Results There were some differences between the nominal values and the measured mean magnetic induction intensities. In a few groups the differences were close to 20％. There were also differences within the same group. The magnetic induction intensities of the two polar surfaces were not always equal for the same magnet, and there were large differences among individual magnets.Conclusions The intensities of magnetic sources must be measured before use to ensure the consistency of magnetic induction intensities in therapeutic applications.

Objective To evaluate the viability of adipocytes after they are subjected to different compressive stress in vitro for improvement of autologous fat graft and its clinical application.Methods Fat grafts were harvested from healthy patients who underwent liposuction for body contouring.Then the fat grafts were randomly divided into 5 experimental groups,including control group without any compressive stress,and continuous compressive stress groups (0,25,50,75,and 100 kPa),and the glucose transport test was performed at days 1,2,3 and 4.An MTT assay was also performed after 4 days with continuous compressive stress in each group with the same experimental protocol for control.Routine histological examination was done in all groups to examine possible structural destruction after compressive stress.Results As compared with the control group,the glucose transport test showed transported glucose concentration decreased with an increase in compressive stress in all of the other four groups (P＜0.01),and this effect would increase with action time.MTT assay showed absorbance (A492nm) also decreased with an increase in compressive stress in four days (P＜0.05),the similar fndings of MTT assay on the viability of fat grafts in all five groups and correlated with the glucose transport test (r=0.838,P＜0.01).Histology showed significantly distorted and fractured adipocytes and cell injury rate was to raise with an increase in compressive stress.Conclusions Our study demonstrates the harmful effect on the viability of fat grafts with an increase in compressive stress and therefore we should reduce this effect in clinical application of fat grafts.

Objective To observe the effects of permanent magnetic fields with different magnetic inductions on oxidative damage to human brain microvascular endothelial cells (HBMECs) under normal and hypoxic conditions. Methods HBMECs were cultured in vitro under normal and hypoxic conditions,then divided into a control group and groups receiving magnetic induction at 8.1,16.5,20.3,26.0,27.3,62.5,110.7 and 215.6 mT.Changes in superoxide dismutase (SOD) activity and malondialdehyde (MDA) content in each group were measured 72 h after exposure to the magnetic fields. Results Under normal conditions the SOD activities of the magnetic groups were not significantly different from that of the control group. Only the MDA content of the 215.6 mT group was statistically different (slightly higher) than that of the control group (P ＜ 0.05 ).Under hypoxic conditions,there was again no statistically significant difference in SOD activity,but the MDA content of the 110.7 mT group was significantly lower. Conclusions Under normal conditions,a 215.6 mT permanent magnetic field has an effect on MDA in HBMECs; under hypoxic conditions a 110.7 mT permanent magnetic field has such an effect.

Objective To explore the impacts of magnetic fields of different intensities on the superoxide dismutase (SOD) activity and malondialdchvde (MDA) levels in rat pancreatic islet cells under normal and hypoxic conditions.Methods Rat pancreatic islet cells were culured,and after 3 days were subjected to a magnetic field of either 44.8 mT,90.6 mT or 182.1 mT under either normal or hypoxic conditions.Control cells received no magnetic field exposure,SOD activity and MDA level were measured after 72 hr.Results The cultured cells grew linearly with optical density (OD) of 0.067 ± 0.021 after 2 days and 0.449 ± 0.113 afier 5 days.SOD activity was significantly lower in the three magnetic field intervention groups than in the control group.Under hypoxic culture conditions,in all the magnetic field intervention groups SOD activity increased at first and then deereased.Under normal culture conditions,MDA content was significantly higher in the 182.1 mT group than in the control group.In the other two groups it was significantly lower.Conclusion Magnetic field exposure can cause oxidative damage to pancreatic islet cells,at least rat cells in culture.Under hypoxic culture conditions a magnetic field can inhibit such damage.

Objective To observe the biological effects of magnetic fields of different intensities on microvascular endothelial cells in the human brain (HBMECs).Methods HBMECs were cultured in vitro under normal conditions and randomly divided into a control group and several magnetic induction groups——26 mT,62.5 mT,110.7 mT and 215.6 mT at the center pole.Any changes to the cytomembranes were observed 72 h after planking using the lactate dehydrogenase (LDH) method.Superoxide dismutase and malondialdehyde methods were used to detect cellular oxidation due to the magnetic field.An inverted microscope was used to observe any changes in cell morphology,and flow cytometry was employed to detect cell apoptosis.Results Compared with the control group,the LDH value of the 215.6 mT group was significantly higher,but there were no significant differences in oxidative damage,apoptosis or morphology observed.Moreover,there were no significant differences between the controls and the 26 mT,62.5 mT and 110.7 mT groups in any of the above measurements.Conclusion Magnetic fields of different intensity have different biological effects on HBMECs.A 215.6 mT magnetic field influences their cell membranes but causes no oxidative damage,cell apoptosis or morphological changes.These observations and the mechanism need further exploration.

Objective To investigate the characteristic changes of biochemical markers of mineral metabolism, vascular calcification, and renal osteodystrophy in an adenine-induced rat model of chronic kidney disease (CKD). Methods A total of 20 male Sprague Dawley rats (SD rats) were randomly divided into two groups: the normal group fed with a diet without adenine, and the CKD group fed with an adenine-containing diet (7. 5 g/kg) for the first 4 weeks and then a diet without adenine for the following 2 weeks. At the end of the 2nd week, serum biochemical markers were detected. At the end of the 6th week, the SD rats were sacrificed and serum biochemical markers were detected once again. The aortas were collected for pathological examination and detection of vascular calcium and phosphorus contents. Femurs and the fifth lumbar vertebrae were taken for bone mineral density (BMD) measurement and bone histomorphometric analysis. Results At the end of the 2nd and 6th weeks, compared with the normal control group, the levels of serum creatinine, urea nitrogen, phosphorus and parathyroid hormone (PTH) in the CKD group were significantly increased (P＜0. 05 or P＜ 0. 01), and the level of serum calcium was significantly decreased (P＜ 0. 05 or P＜ 0. 01). Medial layer vascular calcification of the aorta occurred in 50％ of the rats in the CKD group, but was not observed in the normal control group. Vascular calcium and phosphorus contents were significantly higher in the CKD group compared with the normal control group (P＜ 0. 05). The BMD of total femur, cortical and trabecular bone tissues of the femur, and the fifth lumbar vertebra was significantly decreased in the CKD group (P＜ 0. 05 or P＜ 0. 01). The histomorphometric analysis showed that both bone resorption and bone formation of the trabecular bone in the CKD group were increased, indicating a high bone turnover status. The volumes of both trabecular and cortical bones of rats in the CKD group were significantly lower than that of the normal control group (P ＜ 0. 05 or P ＜ 0. 01). However, the trabecular bone mineralization was not significantly different between the two groups. Conclusions The adenine-induced rat model of chronic kidney disease (CKD) established in this study shows reduced serum calcium and increased serum phosphorus and PTH, and medial layer vascular calcification of the aorta. With respect to renal osteodystrophy, this model shows a high trabecular bone turnover, normal trabecular bone mineralization, and low bone volume of cortical and trabecular bone, which meets the characteristics of osteitis fibrosa. This model may become a useful tool for future study of chronic kidney disease-mineral and bone disorder (CKD-MBD).

Objective:To investigate the effects of miRNA-143-3p on the proliferation, migration and invasion of keloid fibroblasts (KFB) and the possible mechanism.Methods:KFB and normal skin fibroblasts (NFB) were isolated and cultured. The expression of miRNA-143-3p and integrin β5 (ITGB5) at mRNA level in KFB and NFB were detected by RT-qPCR. Western blot was performed to measure the expression of ITGB5 at protein level. After overexpressing miRNA-143-3p or suppressing ITGB5 expression in KFB cells, MTT assay, Transwell assay, RT-qPCR and Western blot were used to detect the effects on the proliferation, migration and invasion of KFB and the expression of related proteins. Dual-luciferase reporter gene assay was used to validate the targeting relationship between miRNA-143-3p and ITGB5.Results:Compared with NFB, KFB showed down-regulated miRNA-143-3p expression and up-regulated expression of ITGB5 at both mRNA and protein levels. The proliferation, migration and invasion of KFB were inhibited after overexpressing miRNA-143-3p or suppressing ITGB5 expression. Moreover, miRNA-143-3p could negatively regulate ITGB5 expression and overexpression of ITGB5 reversed the effects of miRNA-143-3p overexpression on KFB proliferation, migration and invasion.Conclusions:This study suggested that miRNA-143-3p could inhibit the proliferation, migration and invasion of KFB through down-regulating ITGB5 expression.