In this study, we present an assessment of human-body exposure to an electromagnetic field at frequencies ranging from 10 GHz to 1 THz. The energy absorption and temperature elevation were assessed ...by solving boundary value problems of the one-dimensional Maxwell equations and a bioheat equation for a multilayer plane model. Dielectric properties were measured in vitro at frequencies of up to 1 THz at body temperature. A Monte Carlo simulation was conducted to assess variations of the transmittance into a skin surface and temperature elevation inside a body by considering the variation of the tissue thickness due to individual differences among human bodies. Furthermore, the impact of the dielectric properties of adipose tissue on temperature elevation, for which large discrepancies between our present measurement results and those in past works were observed, was also examined. We found that the dielectric properties of adipose tissue do not impact on temperature elevation at frequencies over 30 GHz. The potential risk of skin burn was discussed on the basis of the temperature elevation in millimeter-wave and terahertz-wave exposure. Furthermore, the consistency of the basic restrictions in the international guidelines set by ICNIRP was discussed.
International guidelines/standards for human protection from electromagnetic fields have been revised recently, especially for frequencies above 6 GHz where new wireless communication systems have ...been deployed. Above this frequency a new physical quantity 'absorbed/epithelial power density' has been adopted as a dose metric. Then, the permissible level of external field strength/power density is derived for practical assessment. In addition, a new physical quantity, fluence or absorbed energy density, is introduced for protection from brief pulses (especially for shorter than 10 s). These limits were explicitly designed to avoid excessive increases in tissue temperature, based on electromagnetic and thermal modeling studies but supported by experimental data where available. This paper reviews the studies on the computational modeling/dosimetry which are related to the revision of the guidelines/standards. The comparisons with experimental data as well as an analytic solution are also been presented. Future research needs and additional comments on the revision will also be mentioned.
In modern communication systems including the fifth-generation mobile communication system (5G), quasi-millimeter, and millimeter wave frequencies above 6 GHz are utilized. At these frequencies, the ...incident power density is employed as a metric to assess the compliance of wireless devices to human exposure limits in international guidelines and national regulations. In this article, the performance of the inverse source method (ISM) for incident power density evaluation is investigated in terms of accuracy and operational costs, i.e., measurement and computational costs. The ISM is based on the surface equivalence theorem, and it reconstructs the incident power density close to the device under test from a field measured in a more distant region. The comparison of the performance between the ISM and the conventional plane-wave spectrum method by computational simulation shows that the ISM has an advantage over the conventional method in robustness to the truncation of the measurement region. The ISM reduces the number of measurement points to a quarter for the reconstruction of the spatially averaged incident power density in an error less than 0.4 dB. These findings in the computational simulations are also validated by the measurements of a standard horn antenna and array antennas operated at 28 GHz.
This article reviews recent standardization activities and scientific studies related to the assessment of human exposure to electromagnetic fields (EMF). The differences of human exposure standards ...and assessment of consumer products and medical applications are summarized. First, we reviewed human body modeling and tissue dielectric properties. Then, we explain the rationale of current exposure standards from the viewpoint of EMF and the standardization process for product compliance based on these exposure standards. The assessment of wireless power transfer, as an example of emerging wireless devices, and environmental EMFs in our daily lives are reviewed. Safety in magnetic resonance systems, where the EMF exposure is much larger than from typical consumer devices, is also reviewed. Finally, we summarize future research directions and research needs for EMF safety.
AKI is characterized by abrupt and reversible kidney dysfunction, and incomplete recovery leads to chronic kidney injury. Previous studies by us and others have indicated that macrophage infiltration ...and polarization play key roles in recovery from AKI. The role in AKI recovery played by IFN regulatory factor 4 (IRF4), a mediator of polarization of macrophages to the M2 phenotype, is unclear.
We used mice with myeloid or macrophage cell-specific deletion of
(MΦ
) to evaluate Irf4's role in renal macrophage polarization and development of fibrosis after severe AKI.
Surprisingly, although macrophage
deletion had a minimal effect on early renal functional recovery from AKI, it resulted in decreased renal fibrosis 4 weeks after severe AKI, in association with less-activated macrophages. Macrophage
deletion also protected against renal fibrosis in unilateral ureteral obstruction. Bone marrow-derived monocytes (BMDMs) from MΦ
mice had diminished chemotactic responses to macrophage chemoattractants, with decreased activation of AKT and PI3 kinase and increased PTEN expression. PI3K and AKT inhibitors markedly decreased chemotaxis in wild-type BMDMs, and in a cultured macrophage cell line. There was significant inhibition of homing of labeled
BMDMs to postischemic kidneys. Renal macrophage infiltration in response to AKI was markedly decreased in MΦ
mice or in wild-type mice with inhibition of AKT activity.
Deletion of
from myeloid cells protected against development of tubulointerstitial fibrosis after severe ischemic renal injury in mice, due primarily to inhibition of AKT-mediated monocyte recruitment to the injured kidney and reduced activation and subsequent polarization into a profibrotic M2 phenotype.
Renal epidermal growth factor receptor (EGFR) signaling is activated in models of diabetic nephropathy (DN), and inhibition of the EGFR signaling pathway protects against the development of DN. We ...have now determined that in cultured podocytes, high glucose led to increases in activation of EGFR signaling but decreases in autophagy activity as indicated by decreased beclin-1 and inhibition of LC3B autophagosome formation as well as increased rubicon (an autophagy inhibitor) and SQSTM1 (autophagy substrate). Either genetic (small interfering siEGFR) or pharmacologic (AG1478) inhibition of EGFR signaling attenuated the decreased autophagy activity. In addition, rubicon siRNA knockdown prevented high glucose-induced inhibition of autophagy in podocytes. We further examined whether selective EGFR deletion in podocytes affected the progression of DN in type 2 diabetes. Selective podocyte EGFR deletion had no effect on body weight or fasting blood sugars in either
mice or
;
mice, a model of accelerated type 2 DN. However selective podocyte EGFR deletion led to relative podocyte preservation and marked reduction in albuminuria and glomerulosclerosis, renal proinflammatory cytokine/chemokine expression, and decreased profibrotic and fibrotic components in
;
mice. Podocyte EGFR deletion led to decreased podocyte expression of rubicon, in association with increased podocyte autophagy activity. Therefore, activation of EGFR signaling in podocytes contributes to progression of DN at least in part by increasing rubicon expression, leading to subsequent autophagy inhibition and podocyte injury.
Mesenchymal stem cells (MSCs) exert their anti-inflammatory and anti-fibrotic effects by secreting various humoral factors. Interferon-gamma (IFN-γ) can enhance these effects of MSCs, and enhancement ...of regulatory T (Treg) cell induction is thought to be an underlying mechanism. However, the extent to which Treg cell induction by MSCs pretreated with IFN-γ (IFN-γ MSCs) ameliorates renal fibrosis remains unknown. In this study, we investigated the effects of Treg cell induction by IFN-γ MSCs on renal inflammation and fibrosis using an siRNA knockdown system. Administration of IFN-γ MSCs induced Treg cells and inhibited infiltration of inflammatory cells in ischemia reperfusion injury (IRI) rats more drastically than control MSCs without IFN-γ pretreatment. In addition, administration of IFN-γ MSCs more significantly attenuated renal fibrosis compared with control MSCs. Indoleamine 2,3-dioxygenase (IDO) expression levels in conditioned medium from MSCs were enhanced by IFN-γ pretreatment. Moreover, IDO1 knockdown in IFN-γ MSCs reduced their anti-inflammatory and anti-fibrotic effects in IRI rats by reducing Treg cell induction. Our findings suggest that the increase of Treg cells induced by enhanced secretion of IDO by IFN-γ MSCs played a pivotal role in their anti-fibrotic effects. Administration of IFN-γ MSCs may potentially be a useful therapy to prevent renal fibrosis progression.
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IZUM, KILJ, NUK, PILJ, PNG, SAZU, UL, UM, UPUK
H3K9 methyltransferase G9a is reportedly induced by transforming growth factor-β1 (TGF-β1) and has an important role in the development of epithelial–mesenchymal transposition in cancer cells. Since ...the transcriptional activity of the Klotho gene is regulated by H3K9 modification, we investigated the effects of G9a on renal fibrosis and klotho expression. G9a levels were significantly upregulated by day 7 in the kidneys of unilateral ureteral-obstructed mice, but this was inhibited by TGF-β1-neutralizing antibody. Administration of G9a small interfering RNA not only decreased α-smooth muscle actin and fibronectin but also increased klotho expression in the ureteral-obstructed mice. Similarly, intraperitoneal injection of BIX01294, a specific inhibitor of G9a, showed beneficial effects on renal fibrosis and klotho expression with decreased monomethylation of H3K9 (me1). In in vitro experiments, BIX01294 also inhibited TGF-β1-induced fibrotic changes and klotho downregulation along with suppressed H3K9me1. In human kidney biopsy specimens, areas of G9a immunostaining correlated positively with H3K9me1 levels, as well as fibrotic markers, but correlated negatively with klotho expression. Thus, TGF-β1-induced G9a has an important role in the progression of renal fibrosis and reduced klotho expression through H3K9me1.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Transforming growth factor-β1 (TGF-β1) is a major mediator of peritoneal fibrosis and reportedly affects expression of the H3K4 methyltransferase, SET7/9. SET7/9-induced H3K4 mono-methylation ...(H3K4me1) critically activates transcription of fibrosis-related genes. In this study, we examined the effect of SET7/9 inhibition on peritoneal fibrosis in mice and in human peritoneal mesothelial cells (HPMCs). We also examined SET7/9 expression in nonadherent cells isolated from the effluent of peritoneal dialysis (PD) patients. Murine peritoneal fibrosis was induced by intraperitoneal injection of methylglyoxal (MGO) into male C57/BL6 mice over 21 days. Sinefungin, a SET7/9 inhibitor, was administered subcutaneously just before MGO injection (10 mg/kg). SET7/9 expression was elevated in both MGO-injected mice and nonadherent cells isolated from the effluent of PD patients. SET7/9 expression was positively correlated with dialysate/plasma ratio of creatinine in PD patients. Sinefungin was shown immunohistochemically to suppress expression of mesenchymal cells and collagen deposition, accompanied by decreased H3K4me1 levels. Peritoneal equilibration tests showed that sinefungin attenuated the urea nitrogen transport rate from plasma and the glucose absorption rate from the dialysate. In vitro, sinefungin suppressed TGF-β1-induced expression of fibrotic markers and inhibited H3K4me1. These findings suggest that inhibiting the H3K4 methyltransferase SET7/9 ameliorates peritoneal fibrosis.
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DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
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