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Abstract In this work, it is proposed the development a new monopole directional antenna, bioinspired in elliptical leaf, with cut by golden ratio, for 4G band application, by the use of the technique of the cut of the radiating element for the increasing of the antenna perimeter, being the first work to use this technique in a bioinspired antenna, promotes resonance frequency turned, and reconfiguring of the antenna parameters as bandwidth, radiation pattern and gain, with the use of the reflector near to the group plane, without the insertion of active devices as the pin diode or change in radiating element. The shape antenna is generated by Gielis formula, built in FR4 substrate, with cuts calculated by golden ratio. To compare the results of the bioinspired monopole on the elliptical sheet, a square-shaped monopole antenna was designed, simulated and measured, the structures were designed in the MATLAB software version 2015(b) and the simulations were performed in the Ansys software version 2016. In the results compared between the square monopole and the bioinspired antenna in the elliptical sheet, it can be seen that the measured bioinspired antenna, compared to the square monopole, presented a bandwidth reduction of 77.27%, a more compact structure, with a reduction of 98%, covering the wireless local area network, and long-time evolution 4G at 2.5 GHz. The proposed technique uses a reflector on the ground plane, to change the parameters of the monopole planar antenna, of omnidirectional radiation pattern to a directional, maintaining the characteristics of the broadband, half-power beamwidth great than 100°, with high current density, and similar gain of a directional antenna. From the results, it has been observed that the elliptical leaf monopole antenna shows broadband characteristics, with a half-power beamwidth of 128°, wideband, the bandwidth of 500 MHz, a gain of 6.28 dBi, a current density of 13.01 A/m2, and circular polarization.

In the last years increasing attention has been given to the connection between genotype/phenotype and cardiovascular events in subjects with familial hypercholesterolemia (FH). MicroRNAs (miRs) bound to high-density lipoprotein (HDL) may contribute to better discriminate the cardiovascular risk of FH subjects. Our aim was to evaluate the HDL-miR panel in heterozygous FH (HeFH) patients with an LDLR null or defective mutation and its association with pulse wave velocity (PWV). We evaluated lipid panel, HDL-miR panel and PWV in 32 LDLR null mutation (LDLR-null group) and 35 LDLR defective variant (LDLR-defective group) HeFH patients. HDL-miR-486 and HDL-miR-92a levels were more expressed in the LDLR-null group than the LDLR-defective group. When we further stratified the study population into three groups according to both the LDLR genotype and history of ASCVD (LDLR-null/not-ASCVD, LDLR-defective/not-ASCVD and LDLR/ASCVD groups), both the LDLR/ASCVD and the LDLR-null/not-ASCVD groups had a higher expression of HDL-miR-486 and HDL-miR-92a than the LDLR-defective/not-ASCVD group. Finally, HDL-miR-486 and HDL-miR-92a were independently associated with PWV. In conclusion, the LDLR-null group exhibited HDL-miR-486 and HDL-miR-92a levels more expressed than the LDLR-defective group. Further studies are needed to evaluate these HDL-miRs as predictive biomarkers of cardiovascular events in FH.

Statins are a class of drugs widely prescribed as frontline therapy for lowering plasma LDL-cholesterol in cardiovascular risk prevention. Several clinical reports have recently suggested an increased risk of type 2 diabetes associated with chronic use of these drugs. The pathophysiology of this effect remains to be fully elucidated but impaired β-cell function constitutes a potential mechanism. The aim of this study was to explore the effect of a chronic treatment with lipophilic and hydrophilic statins on β-cell function, using human pancreatic islets and rat insulin-secreting INS-1 cells; we particularly focused on the role of mitochondria and oxidative stress. The present study demonstrates, for the first time, that atorvastatin (lipophilic) but not pravastatin (hydrophilic) affected insulin release and mitochondrial metabolism due to the suppression of antioxidant defense system and induction of ROS production in pancreatic β-cell models. Mevalonate addition and treatment with a specific antioxidant (N-AcetylCysteine) effectively reversed the observed defects. These data demonstrate that mitochondrial oxidative stress is a key element in the pathogenesis of statin-related diabetes and may have clinical relevance to design strategies for prevention or reduction of statin induced β-cell dysfunction and diabetes in patients treated with lipophilic statins.