Improving the Covertness in the Physical-Layer Authentication

A well-designed Physical-Layer Authentication(PLA)scheme should consider three properties:covertness,robustness,and security.However,the three properties always cause some dilemmas,e.g.,higher covertness leading to lower robustness.This paper concerns the problem of improving the covertness without sacrificing the robustness.This problem is important because of the following reasons:reducing the errors in recovered source message,improving the security,and ease of constructing a multi-factor authentication system.In this paper,we propose three covert PLA schemes to address the problem.In the first scheme,we improve the covertness by reducing the modification ratio on the source message based on an encoding mechanism.In the second scheme,we improve the covertness by optimizing the superimposing angle,which maximizes the minimum distance between the tagged symbols and the boundary line of the demodulation decision for the source message.In the third scheme,referred to as the hybrid scheme,we further improve the covertness by jointly using the advantages of both the above two schemes.Our experimental results show that when the SNR at a legitimate receiver is 25 dB,as compared with the prior scheme,the first scheme improves the covertness by 17:74%,the second scheme improves the covertness by 28:79%,and the third scheme improves the covertness by 32:09%,while they have similar robustness as Received:Aug.07,2020 Revised:Sep.08,2020 Editor:Nanrun Zhou that of the prior scheme.

Androgen receptor inhibits the hair follicle induction potential of dermal papilla cells by binding with Tcf4 at the A574 binding site

Androgenic alopecia(AGA)is the most common type of clinical alopecia.Androgen receptor(AR)is the most logical candidate gene for regulating the occurrence of AGA.Dermal papilla cells(DPCs)are a special kind of mesenchymal cells,located in the hair bulb of hair follicles.DPCs play a role in maintaining and inducing the periodic cycling of hair follicles,and are considered as a key cell target of androgen in hair follicles.

Wnt4 increases the thickness of the epidermis in burn wounds by activating canonical Wnt signalling and decreasing the cell junctions between epidermal cells

Background:Burn wound healing is a complex process and the role of Wnt ligands varies in this process.Whether and how Wnt4 functions in burn wound healing is not well understood.In this study,we aim to reveal the effects and potential mechanisms of Wnt4 in burn wound healing.Methods:First,the expression of Wnt4 during burn wound healing was determined by immunoflu-orescence,Western blotting and qPCR.Then,Wnt4 was overexpressed in burn wounds.The healing rate and healing quality were analysed by gross photography and haematoxyline and eosin staining.Collagen secretion was observed by Masson staining.Vessel formation and fibroblast distribution were observed by immunostaining.Next,Wnt4 was knocked down in HaCaT cells.The migration of HaCaT cells was analysed by scratch healing and transwell assays.Next,the expression ofβ-catenin was detected by Western blotting and immunofluorescence.The binding of Frizzled2 and Wnt4 was detected by coimmunoprecipitation and immunofluorescence.Finally,the molecular changes induced by Wnt4 were analysed by RNA sequencing,immunofluorescence,Western blotting and qPCR in HaCaT cells and burn wound healing tissues.Results:The expression of Wnt4 was enhanced in burn wound skin.Overexpression of Wnt4 in burn wound skin increased the thickness of epidermis.Collagen secretion,vessel formation and fibroblast distribution were not significantly impacted by Wnt4 overexpression.When Wnt4 was knocked down in HaCaT cells,the ratio of proliferating cells decreased,the ratio of apoptotic cells increased and the ratio of the healing area in the scratch healing assay to the number of migrated cells in the transwell assay decreased.The nuclear translocation ofβ-catenin decreased in shRNA of Wnt4 mediated by lentivirus-treated HaCaT cells and increased in Wnt4-overexpressing epidermal cells.RNA-sequencing analysis revealed that cell junction-related signalling pathways were significantly impacted by Wnt4 knockdown.The expression of the cell junction proteins was decreased by the overexpression of Wnt4.Conclusions:Wnt4 promoted the migration of epidermal cells.Overexpression of Wnt4 increased the thickness of the burn wound.A potential mechanism for this effect is that Wnt4 binds with Frizzled2 and increases the nuclear translocation ofβ-catenin,thus activating the canonical Wnt signalling pathway and decreasing the cell junction between epidermal cells.