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This paper explores the potential application of simultaneously transmitting and reflecting reconfigurable intelligent surface (STAR‐RIS) in improving the physical layer security (PLS) of millimetre wave (mmWave) non‐orthogonal multiple access (NOMA) uplink communications. In particular, the legitimate users on both sides of STAR‐RIS send confidential information simultaneously to the base station (BS) while keeping it secret from the eavesdroppers near the BS by exploiting the STAR‐RIS to proactively regulate the electromagnetic propagation environment. By jointly designing the transmit power, the active beamforming at the BS, and the reflecting/transmitting coefficients at the STAR‐RIS, the authors' goal is to maximize the minimum secrecy capacity subject to the successive interference cancellation decoding order constraints. Due to the non‐convexity of the formulated problem, an efficient algorithm is proposed by capitalizing on alternating optimization, a penalty‐based approach, successive convex approximation, and semi‐definite relaxation. Firstly, a two‐layer iterative algorithm based on the penalty for the joint beamforming optimization sub‐problem is proposed. Then, the non‐convex problem is transformed into a convex positive semi‐definite programming problem for the transmit power sub‐problem. Numerical simulation results reveal that the STAR‐RIS‐aided system has more tremendous advantages and effectiveness in improving the PLS of mmWave NOMA uplink communication compared with the benchmark schemes. [ABSTRACT FROM AUTHOR]

The secure communication scheme based on physical layer non‐reconciled keys receives extensive attention due to its high encryption rate. However, the mismatched secret bit sequences between the two users leads to higher BER and lower coding efficiency for this type of scheme. To solve this problem, this paper proposes an efficient and secure communication scheme for OFDM system with non‐reconciled keys. Initially, an adaptive coding method is designed to encode information blocks with different code rates to improve the overall efficiency. Then, on this basis, a sorting xor encryption algorithm is designed to reduce the bit error rate by sorting the channel estimation value and mapping them to corresponding sub‐channels. Theoretical analysis and simulation results indicate that this scheme can effectively reduce the bit error rate and improve the efficiency of information coding compared to the existing method. [ABSTRACT FROM AUTHOR]

Targeting the androgen receptor (AR) signalling pathway remains the main therapeutic option for advanced prostate cancer. However, resistance to AR‐targeting inhibitors represents a great challenge, highlighting the need for new therapies. Activation of the PI3K/AKT pathway and increased expression of histone deacetylases (HDACs) are common aberrations in prostate cancer, suggesting that inhibition of such targets may be a viable therapeutic strategy for this patient population. Previous reports demonstrated that combination of PI3K inhibitors (PI3KIs) with histone deacetylase inhibitors (HDACIs) resulted in synergistic antitumour activities against preclinical models of prostate cancer. In this study, we demonstrate that the novel dual PI3K and HDAC inhibitor CUDC‐907 has promising antitumour activity against prostate cancer cell lines in vitro and castration‐resistant LuCaP 35CR patient‐derived xenograft (PDX) mouse model in vivo. CUDC‐907‐induced apoptosis was partially dependent on Mcl‐1, Bcl‐xL, Bim and c‐Myc. Further, down‐regulation of Wee1, CHK1, RRM1 and RRM2 contributed to CUDC‐907‐induced DNA damage and apoptosis. In the LuCaP 35CR PDX model, treatment with CUDC‐907 resulted in significant inhibition of tumour growth. These findings support the clinical development of CUDC‐907 for the treatment of prostate cancer. [ABSTRACT FROM AUTHOR]

Ischemic heart disease (IHD) is the main cause of death and a major public health problem in the world. The traditional herbal medicinal formula Guan-Xin-Er-Hao (GXEH) has been used in China and East Asia for the treatment of coronary heart disease, however, the underlying cardioprotection mechanisms remain unclear. To make clear the antiischemic mechanism involved, GXEH was orally administered to 15 healthy volunteers. Heart rates (HR), blood pressure and coronary flow (CF) velocity before and 1 h after a single oral dose of GXEH were observed and compared. It was demonstrated that the oral administration of GXEH increased CF acutely in a dose-dependent manner without modification of systemic hemodynamic parameters. Moreover, the myocardial protection function of GXEH was also experimentally examined in ischemia-reperfusion (I/R) rat models. Apoptosis was measured quantitatively by the terminal transferase UTP nick end-labeling (TUNEL) method and confirmed by caspase-3 activity. The infarct size and TUNEL-positive cells of GXEH-treated group (20 g/kg) were reduced significantly, which was consistent with the decreased caspase-3 activity. These suggest that GXEH protects hearts from ischemia injury by increasing CF and reduces infarct size by inhibiting myocardial apoptosis. [ABSTRACT FROM AUTHOR]