Multi-Mode Dual-Polarized Cavity Backed Patch Antenna Array for 5G Mobile Devices

Abstract This paper proposes a dual‐polarised cavity backed patch antenna for next generation phased arrays for mobile handsets. The antenna exhibits multi‐band performance, allowing to cover the 5G bands n257 (26.5–29.5 GHz), n258 (24.25–27.5 GHz), n261 (27.5–28.35 GHz) and a portion of band n260 (37–40 GHz). Two orthogonal modes are excited in the substrate integrated waveguide (SIW) cavity and show similar impedance matching and symmetric radiation patterns. A parasitic element is introduced on top of the cavity and shifted off‐centre to improve the port‐to‐port isolation and guide the main beam. A parametric study of the antenna dimensions is conducted to verify the multi‐resonance operating mechanism. The design is validated by the measurements of the fabricated four‐element array. The array scanning angle is from −35° to 38° for V‐pol and from −29° to 31° for H‐pol at 28 GHz, where the realised gain raises from 8 to 12 dBi

A Study on EMF Exposure Assessments With Different Metrics for User Equipment Antennas at 6 and 10 GHz

User equipment (UE) needs to comply with regulations limiting the exposure of the human body to electromagnetic fields (EMFs). In this paper, three exposure metrics including specific absorption rate (SAR), incident power density, and absorbed power density are quantified for different UE antenna designs. The study is conducted for three antennas - planar dipole, inverted-F antenna (IFA), and planar inverted-F antenna (PIFA), at two frequencies - 6 and 10 GHz, and for evaluation distances from 4 to 10 mm, which are within or close to the antenna’s reactive near field. The exposure ratios of the metrics are quantified according to the relevant EMF limit values. For validation purposes, prototypes are fabricated, and SAR and incident power density are measured. The average difference between the numerical and experimental results is 0.4 dB for SAR and 0.9 dB for the incident power density, meaning that good agreement between simulations and measurements is obtained. The study provides valuable input for EMF as- sessment requirements and test methodologies for emerging technologies at or close to the transition frequency between different exposure metrics

Oxaliplatin Neurotoxicity Involves Peroxisome Alterations. PPARc Agonism as Preventive Pharmacological Approach

The development of neuropathic syndromes is an important, dose limiting side effect of anticancer agents like platinum derivates, taxanes and vinca alkaloids. The causes of neurotoxicity are still unclear but the impairment of the oxidative equilibrium is strictly related to pain. Two intracellular organelles, mitochondria and peroxisomes cooperate to the maintaining of the redox cellular state. Whereas a relationship between chemotherapy-dependent mitochondrial alteration and neuropathy has been established, the role of peroxisome is poor explored. In order to study the mechanisms of oxaliplatin-induced neurotoxicity, peroxisomal involvement was evaluated in vitro and in vivo. In primary rat astrocyte cell culture, oxaliplatin (10 µM for 48 h or 1 µM for 5 days) increased the number of peroxisomes, nevertheless expression and functionality of catalase, the most important antioxidant defense enzyme in mammalian peroxisomes, were significantly reduced. Five day incubation with the selective Peroxisome Proliferator Activated Receptor-γ (PPAR-γ) antagonist G3335 (30 µM) induced a similar peroxisomal impairment suggesting a relationship between PPARγ signaling and oxaliplatin neurotoxicity. The PPARγ agonist rosiglitazone (10 µM) reduced the harmful effects induced both by G3335 and oxaliplatin. In vivo, in a rat model of oxaliplatin induced neuropathy, a repeated treatment with rosiglitazone (3 and 10 mg kg(-1) per os) significantly reduced neuropathic pain evoked by noxious (Paw pressure test) and non-noxious (Cold plate test) stimuli. The behavioral effect paralleled with the prevention of catalase impairment induced by oxaliplatin in dorsal root ganglia. In the spinal cord, catalase protection was showed by the lower rosiglitazone dosage without effect on the astrocyte density increase induced by oxaliplatin. Rosiglitazone did not alter the oxaliplatin-induced mortality of the human colon cancer cell line HT-29. These results highlight the role of peroxisomes in oxaliplatin-dependent nervous damage and suggest PPARγ stimulation as a candidate to counteract oxaliplatin neurotoxicity

Different apoptotic pathways activated by oxaliplatin in primary astrocytes vs. colo-rectal cancer cells

Oxaliplatin-based chemotherapy improves the outcomes of metastatic colorectal cancer patients. Its most significant and dose-limiting side effect is the development of a neuropathic syndrome. The mechanism of the neurotoxicity is unclear. The limited knowledge about differences existing between neurotoxic and antitumor effects hinders the discovery of effective and safe adjuvant therapies. In vitro, we suggested cell-specific activation apoptotic pathways in normal nervous cells (astrocytes) vs. colon-cancer cells (HT-29). In the present research we compared the apoptotic signals evoked by oxaliplatin in astrocytes and HT-29 analyzing the intrinsic and extrinsic apoptotic pathways. In astrocytes, oxaliplatin induced a mitochondrial derangement measured as cytosolic release of cytochrome C, increase in superoxide anion levels and decreased expression of the antiapoptotic protein Bcl-2. Caspase-8, a main initiator of the extrinsic process remained unaltered. On the contrary, in HT-29 oxaliplatin increased caspase-8 activity and Bid expression, thus activating the extrinsic apoptosis, while the Bcl-2 increased expression blocked the mitochondrial damage. Data suggest the preferred activation of the intrinsic apoptosis as oxaliplatin damage signaling in normal nervous cells. The extrinsic pathway prevails in tumor cells indicating a possible strategy for planning new molecules to treat oxaliplatin-dependent neurotoxicity without negatively influence chemotherapy