On the other hand, other growth factors such as VEGF, HGF and TGF-b1 were not changed, which suggests that the expression of IGF-1 was rather specific to RF radiation. The increased expression of IGF-1 was validated by Western blot against BCL-2, BAX, and pMAPK1, all of which seem to be targets of IGF-1. RF exposure activates IGF-1 mRNA expression to promote cell survival of hDPCs by Wortmannin increasing the ratio of BCL-2/BAX. CCND1 plays an important role in promoting G1-to-S phase progression. The signals downstream of MAPK related to mitogenesis contain the phosphorylation of transcription factors including JUN, ETS1, and ELK1, such as the cyclin D family. RF exposure could up-regulate the phosphorylation of MAPK1 and subsequently increase the expression of CCND1 as shown in Fig. 1. However, the overall cell cycle progression was not changed in RF-exposed cells, as shown in Fig. 2E. The increased levels of BCL-2 and CCND1 and the phosphorylation of MAPK1 may not be sufficient to induce the proliferation of hDPCs. The expression of BCL-2 and CCND1 and the phosphorylation of MAPK1 are important for cell survival by inhibiting apoptosis. Cell cycle progression requires additional changes in gatekeeper genes such as p53 and Rb for G1/S transition. We could not detect changes in cell cycle distribution in RF-irradiated hDPCs as other type of cells. RF exposure does not induce DNA strand breaks, chromosome aberrations, sister chromatid exchanges, DNA repair synthesis, phenotypic mutation, or transformation such as cancer-like changes. Exposure to RF radiation exerts no detectable effects on cell cycle distribution, cellular migration, or invasion at average SAR values of 2 or 10 W/kg. In contrast, another study noted that RF radiation induced basal cell proliferation and mild skin changes in rat skin cells. A diverse range of opinions exist with regard to whether RF exposure induces cellular change, and the results of these studies depend on the cell type, exposure time, frequency, or radiation dose used. We used higher SAR levels than previous reports, but we did not detect any evidence of oxidative stress. In this study, we demonstrated that RF exposure stimulated hair growth in an ex vivo system and an in vitro model using hDPCs. Our future studies will be focused on investigating the effect of RF radiation using various frequencies and doses to better understand the biological responses. In addition, we need to explore human hair growth on other types of HFs. Interestingly, 1,763 MHz RF radiation at a higher SAR, for example 60 W/kg, hardly showed linear responses in hDPCs and outer root sheath cells, which are keratinocytes of human scalp HFs. From these results, we propose that RF radiation at a specific dose and exposure time could be used to treat human hair disorders such as androgenetic alopecia. Fast and reliable identification of moulds would help manage the growing number of invasive mould infections, a leading cause of morbidity and lethality in immunocompromised patients. Currently, mould identification relies on the macroscopic and microscopic observation of colonies grown on mycological media. Adequate phenotypic identification of moulds requires highly skilled mycologists, who are found in a few reference laboratories.