A Compact Linear Microstrip Patch Beamformer Antenna Array for Millimeter-Wave Future Communication.

5/6G is anticipated to address challenges such as low data speed and high latency in current cellular networks, particularly as the number of users overwhelms 4G and LTE capabilities. This paper proposes a microstrip patch antenna array comprising six radiating patches and utilizing a microstrip line feeding technique to facilitate the compact design crucial for 5G implementation. ROGER 3003, chosen for its advanced and environmentally friendly features, serves as the dielectric material, ensuring suitability for 5G and B5G applications. The designed antenna, evaluated at a resonating frequency of 28.8 GHz with a -10 dB impedance bandwidth of 1 GHz, offers a high gain of 9.19 dBi. Its compact array, cost-effectiveness, and broad impedance and radiation coverage position it as a viable candidate for 5G and future communication applications.

4-Methylcoumarin-[5,6-g]-hesperetin attenuates inflammatory responses in alcoholic hepatitis through PPAR-γ activation.

4-Methylcoumarin-[5,6-g]-hesperetin (4-MCH) is a hesperidin derivative produced by the structural modification of hesperetin. Alcoholic hepatitis (AH) is the origin of many serious liver diseases that are accompanied by hepatic inflammation. In this study, we detected the anti-inflammatory activity of 4-MCH in EtOH fed mice and examined the potential molecular mechanism of this activity. We found that 4-MCH suppressed the release of inflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in primary liver macrophages isolated from mice and in EtOH-treated RAW264.7 cells. In addition, we showed that the expression of peroxisome proliferator-activated receptor-γ (PPAR-γ) was down-regulated in vivo and in vitro in AH. Furthermore, 4-MCH acted as an activator of PPAR-γ, which could therefore ameliorate the inhibitory effects of EtOH on the expression of PPAR-γ. The impairment of PPAR-γ function (T0070907 or PPAR-γ siRNA treatment) resulted in greater inflammation than that in the control group. Conversely, over-expression of PPAR-γ further reduced the release of inflammatory cytokines from EtOH-stimulated RAW264.7 cells. Additional investigations showed that 4-MCH significantly inhibited the phosphorylation of p65. Collectively, these results indicate that 4-MCH alleviated the inflammatory reaction through PPAR-γ activation via the NF-κB-p65 signaling pathway, which regulates the expression of IL-6 and TNF-α in AH.