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Objective: Far infrared radiation has been widely used in a variety of healthcare institutions and clinical research. Previous studies have shown that far infrared radiation can promote blood circulation and enhance the functioning of the immune system. Many patients receiving peritoneal dialysis have been co-treated with far infrared radiation to reduce the occurrence of inflammation. This study seeks to evaluate the effects of far infrared radiation therapy on inflammation.
Method: We used the lipopolysaccharide-induced peritonitis mouse model to study the effect of far infrared radiation treatment. Sixteen mice were randomly divided into two groups, a far infrared radiation treatment group (n = 8) and a non-far infrared radiation treatment group (n = 8). Collected blood samples were studied by analyzing the RNA level of peripheral blood mononuclear cells and the plasma protein levels of interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), and endothelial
nitric oxide synthase (eNOS).
Results: The administration of far infrared radiation inhibited the RNA levels of interleukin-6 and TNF-α after stimulation by lipopolysaccharide. The far infrared radiation treatment inhibited the endothelial nitric oxide synthase RNA levels at 1 h, but the RNA levels returned close to the baseline level after 2 h. In the control group, the endothelial nitric oxide synthase RNA levels were continuously decreasing. The interleukin-6 concentration in the plasma of the far infrared radiation group showed significant inhibition 30 min after lipopolysaccharide stimulation. The tumor necrosis factor alpha RNA concentration in plasma of the far infrared radiation group was significantly reduced 2 h after lipopolysaccharide stimulation.
Conclusion: Far infrared radiation therapy can inhibit interleukin-6 and tumor necrosis factor alpha RNA levels of peripheral blood mononuclear cells and recover endothelial nitric oxide synthase expression. These results demonstrate that far infrared radiation therapy might aid in reducing the level of inflammation experienced by patients going through peritoneal dialysis treatment.

Far infrared radiation, a subdivision of the electromagnetic spectrum, is beneficial for long-term tissue healing, anti-inflammatory effects, growth promotion, sleep modulation, acceleration of microcirculation, and pain relief. We investigated if far infrared radiation is beneficial for renal proximal tubule cell cultivation and renal tissue engineering. We observed the effects of far infrared radiation on renal proximal tubules cells, including its effects on cell proliferation, gene and protein expression, and viability. We also examined the protective effects of far infrared radiation against cisplatin, a nephrotoxic agent, using the human proximal tubule cell line HK-2. We found that daily exposure to far infrared radiation for 30 min significantly increased rabbit renal proximal tubule cell proliferation in vitro, as assessed by MTT assay. Far infrared radiation was not only beneficial to renal proximal tubule cell proliferation, it also increased the expression of ATPase Na+/K+ subunit alpha 1 and glucose transporter 1, as determined by western blotting. Using quantitative polymerase chain reaction, we found that far infrared radiation enhanced CDK5R1, GNAS, NPPB, and TEK expression. In the proximal tubule cell line HK-2, far infrared radiation protected against cisplatin-mediated nephrotoxicity by reducing apoptosis. Renal proximal tubule cell cultivation with far infrared radiation exposure resulted in better cell proliferation, significantly higher ATPase Na+/K+ subunit alpha 1 and glucose transporter 1 expression, and significantly enhanced expression of CDK5R1, GNAS, NPPB, and TEK. These results suggest that far infrared radiation improves cell proliferation and differentiation. In HK-2 cells, far infrared radiation mediated protective effects against cisplatin-induced nephrotoxicity by reducing apoptosis, as indicated by flow cytometry and caspase-3 assay.

Ultraviolet (UV) induces skin photoaging, which is characterized by thickening, wrinkling, pigmentation, and dryness. Collagen, which is one of the main building blocks of human skin, is regulated by collagen synthesis and collagen breakdown. Autophagy was found to block the epidermal hyperproliferative response to UVB and may play a crucial role in preventing skin photoaging. In the present study, we investigated whether far-infrared (FIR) therapy can inhibit skin photoaging via UVB irradiation in NIH 3T3 mouse embryonic fibroblasts and SKH-1 hairless mice. We found that FIR treatment significantly increased procollagen type I through the induction of the TGF-β/Smad axis. Furthermore, UVB significantly enhanced the expression of matrix metalloproteinase-1 (MMP-1) and MMP-9. FIR inhibited UVB-induced MMP-1 and MMP-9. Treatment with FIR reversed UVB-decreased type I collagen. In addition, FIR induced autophagy by inhibiting the Akt/mTOR signaling pathway. In UVB-induced skin photoaging in a hairless mouse model, FIR treatment resulted in decreased skin thickness in UVB irradiated mice and inhibited the degradation of collagen fibers. Moreover, FIR can increase procollagen type I via the inhibition of MMP-9 and induction of TGF-β in skin tissues. Therefore, our study provides evidence for the beneficial effects of FIR exposure in a model of skin photoaging.

• Far infrared radiation (FIR) is currently investigated as a potential therapeutic strategy in various diseases though the mechanism is unknown. Presently, we tested if FIR mediates beneficial effects in a cell model of the neurodegenerative disease spinocerebellar ataxia type 3 (SCA3). SCA3 is caused by a mutation leading to an abnormal polyglutamine expansion (PolyQ) in ataxin-3 protein. The consequent aggregation of mutant ataxin-3 results in disruption of vital cell functions. In this study, neuroblastoma cells (SK-N-SH) was transduced to express either non-pathogenic ataxin-3-26Q or pathogenic ataxin-3-78Q proteins. The cells expressing ataxin-3-78Q demonstrated decreased viability, and increased sensitivity to metabolic stress in the presence rotenone, an inhibitor of mitochondrial respiration. FIR exposure was found to protect against these effects. Moreover, FIR improved mitochondrial respiratory function, which was significantly compromised in ataxin-3-78Q and ataxin-3-26Q expressing cells. This was accompanied by decreased levels of mitochondrial fragmentation in FIR treated cells, as observed by fluorescence microscopy and protein expression analysis. Finally, the expression profile LC3-II, Beclin-1 and p62 suggested that FIR prevent the autophagy inhibiting effects observed in ataxin-3-78Q expressing cells. In summary, our results suggest that FIR have rescuing effects in cells expressing mutated pathogenic ataxin-3, through recovery of mitochondrial function and autophagy.

• This study employed a rat model of sciatic nerve injury to investigate the effects of postoperative low-power far-infrared (FIR) radiation therapy on nerve repair following end-to-end neurorrhaphy. The rat models were divided into the following 3 groups: (1) nerve injury without FIR biostimulation (NI/sham group); (2) nerve injury with FIR biostimulation (NI/FIR group); and (3) noninjured controls (normal group). Walking-track analysis results showed that the NI/FIR group exhibited significantly higher sciatic functional indices at 8 weeks after surgery (P < 0.05) compared with the NI/sham group. The decreased expression of CD4 and CD8 in the NI/FIR group indicated that FIR irradiation modulated the inflammatory process during recovery. Compared with the NI/sham group, the NI/FIR group exhibited a significant reduction in muscle atrophy (P < 0.05). Furthermore, histomorphometric assessment indicated that the nerves regenerated more rapidly in the NI/FIR group than in the NI/sham group; furthermore, the NI/FIR group regenerated neural tissue over a larger area, as well as nerve fibers of greater diameter and with thicker myelin sheaths. Functional recovery, inflammatory response, muscular reinnervation, and histomorphometric assessment all indicated that FIR radiation therapy can accelerate nerve repair following end-to-end neurorrhaphy of the sciatic nerve.

• The aim of this study was to investigate the autonomic responses and central manifestations by peripheral FIR stimulation. Ten subjects (mean ± SD age 26.2 ± 3.52 years) received FIR stimulation at left median nerve territory for 40 min. Electrocardiograph was continuously recorded and heart rate variability (HRV) were analyzed. By using a 3 T-MRI scanner, three sessions of resting-state functional magnetic resonance images (fMRI) were acquired, namely, before (baseline-FIR), immediately after (IA-FIR) and 15 min after FIR was turned off (Post-FIR). The fractional amplitude of low-frequency (0.01-0.08 Hz) fluctuation (fALFF) of each session to evaluate the intensity of resting-brain activity in each session was analyzed. Our results showed that FIR stimulation induced significant HRV responses such as an increasing trend of nLF and LF/HF ratio, while FIR increased fALFF in right superior front gyrus, middle frontal gyrus and decreased the resting brain activity at fusiform gyrus, extrastriae cortex, inferior temporal gyrus and middle temporal gyrus, especially 15 min after FIR was turned off. We conclude that the central manifestation and the autonomic responses are prominent during and after FIR stimulation, which provide important mechanistic explanation on human disorder treated by such energy medicine.

• • OBJECTIVE:
  • Defects in angiogenesis/vasculogenesis or vessel repair are major complications of coronary artery disease (CAD). Endothelial progenitor cells (EPCs) play a fundamental role in postnatal vascular repair and CAD. The role of microRNAs in CAD pathogenesis and their potential as biomarkers remain to be elucidated.

• • APPROACH AND RESULTS:
  • MicroRNA-31 (miR-31) level in both the plasma and EPCs of patients with CAD is found lower. miR-31 regulates EPC activities by targeting FAT atypical cadherin 4 and thromboxane A2 receptor, which show increased expression in CAD EPCs. Overexpressing miR-31 in CAD EPCs rescued their angiogenic and vasculogenic abilities both in vitro and in vivo. When exploring approaches to restore endogenous miR-31, we found that far-infrared treatment enhanced the expression of not only miR-31, but also miR-720 in CAD EPCs. miR-720, which was also decreased in EPCs and the plasma of patients with CAD, stimulated EPC activity by targeting vasohibin 1. The miR720-vasohibin 1 pair was shown to be downstream of FAT atypical cadherin 4, but not of thromboxane A2 receptor. FAT atypical cadherin 4 inhibited miR-720 expression via repression of the planar cell polarity signaling gene four-jointed box 1 (FJX1), which was required for miR-720 expression through a hypoxia-inducible factor 1, α subunit-dependent mechanism. Restoring miR-720 level strengthened activity of CAD EPCs. The miR-31-miR-720 pathway is shown critical to EPC activation and that downregulation of this pathway contributes to CAD pathogenesis. Circulating levels of miR-31, miR-720, and vasohibin 1 have the potential to allow early diagnosis of CAD and to act as prognosis biomarkers for CAD and other EPC-related diseases.

• CONCLUSIONS:
• Manipulating the expression of the miR-31-miR-720 pathway in malfunction EPCs should help develop novel therapeutic modalities.

Far infrared (FIR) irradiation has been widely applied in health promotion. The aims of this study were to investigate the protective effect of FIR irradiation on stressed keratinocytes and the signaling pathways involved. HaCaT was subjected to sorbitol dehydration with or without 40min pretreatment with FIR radiation 4h earlier. Western blots of cell lysates were analyzed for caspase-3, HO-1, BCL2, Bax, ERK, and Akt. The incidence of apoptosis was also assessed by TUNEL staining. Evaluation of cell viability was determined using MTT. mRNAs were extracted and compared using Illumina Human Ref-8 v2 BeadChips. Hyperosomotic injury of HaCaT cells caused by sorbitol resulted in increased cleaved caspase-3 expression and this effect was decreased by FIR pretreatment; these findings were confirmed by TUNEL staining and MTT tests. Pre-treatment with FIR irradiation before sorbitol-induced dehydration significantly upregulated phosphorylated Akt (p-Akt) levels and A6730, an Akt kinase inhibitor (5μM), attenuated the protective effect of FIR irradiation. A microarray study showed FIR irradiation had far less effect at the transcriptional level. FIR pretreatment attenuates apoptosis and cell death in dehydration-stressed cultured keratinocytes through the PI-3K/Akt pathway, this protective effect of FIR irradiation is not at the transcriptional level.

• We have treated a patient with severe phantom limb pain by a novel far infrared ray (FIR) therapy. The patient has suffered persistent and progressively worsening phantom limb pain after amputation ten years ago. He also experienced severe muscle spasm and twitch of stump during the attacks. His phantom limb pain was excruciating and was rated up to 9 by the Visual Analog Pain Scale. Various pain treatment modalities have been used but in vain, including medications and rehabilitation. He also underwent two episodes of sympathectomy, only achieving short-term effects for three months. Then he underwent our new treatment method. We applied FIR to the amputated limb site instead of the stump of the patient for 40 minutes for each treatment session twice a week. One month after the FIR treatment, he felt much improved and rated his phantom pain at 4, and down to 2-3 after two months of treatment. The duration of each phantom limb pain attack has significantly reduced from over 24 hours to only a few minutes or seconds after five months of FIR treatment. During a six-month post-treatment follow-up, his phantom limb pain occurred seldom for only a few seconds at a low 1-2 rating on the pain scale. The analgesic effect of FIR treatment has prevented him from the scheduled third sympathectomy and the risk of heart attack followed by severe twitch of stump. The results of this study demonstrate an easy, non-invasive and effective treatment modality for phantom limb pain.