A gm/ID-Based Low-Power LNA for Ka-Band Applications.

This article presents the design of a low-power low noise amplifier (LNA) implemented in 45 nm silicon-on-insulator (SOI) technology using the gm/ID methodology. The Ka-band LNA achieves a very low power consumption of only 1.98 mW andis the first time the gm/ID approach is applied at such a high frequency. The circuit is suitable for Ka-band applications with a central frequency of 28 GHz, as the circuit is intended to operate in the n257 frequency band defined by the 3GPP 5G new radio (NR) specification. The proposed cascode LNA uses the gm/ID methodology in an RF/MW scenario to exploit the advantages of moderate inversion region operation. The circuit occupies a total area of 1.23 mm2 excluding pads and draws 1.98 mW from a DC supply of 0.9 V. Post-layout simulation results reveal a total gain of 11.4 dB, a noise figure (NF) of 3.8 dB, and an input return loss (IRL) better than 12 dB. Compared to conventional circuits, this design obtains a remarkable figure of merit (FoM) as the LNA reports a gain and NF in line with other approaches with very low power consumption.

Optomechanical realization of the bosonic Kitaev chain.

The fermionic Kitaev chain is a canonical model featuring topological Majorana zero modes1. We report the experimental realization of its bosonic analogue2 in a nano-optomechanical network, in which the parametric interactions induce beam-splitter coupling and two-mode squeezing among the nanomechanical modes, analogous to hopping and p-wave pairing in the fermionic case, respectively. This specific structure gives rise to a set of extraordinary phenomena in the bosonic dynamics and transport. We observe quadrature-dependent chiral amplification, exponential scaling of the gain with system size and strong sensitivity to boundary conditions. All these are linked to the unique non-Hermitian topological nature of the bosonic Kitaev chain. We probe the topological phase transition and uncover a rich dynamical phase diagram by controlling interaction phases and amplitudes. Finally, we present an experimental demonstration of an exponentially enhanced response to a small perturbation3,4. These results represent the demonstration of a new synthetic phase of matter whose bosonic dynamics do not have fermionic parallels, and we have established a powerful system for studying non-Hermitian topology and its applications for signal manipulation and sensing.

Nakazawaea atacamensis f.a., sp. nov. a novel nonconventional fermentative ascomycetous yeast species from the Atacama Desert.

In this study, we describe Nakazawaea atacamensis f. a., sp. nov., a novel species obtained from Neltuma chilensis plant samples in Chile's hyperarid Atacama Desert. In total, three strains of N. atacamensis were obtained from independent N. chilensis samples (synonym Prosopis chilensis, Algarrobo). Two strains were obtained from bark samples, while the third strain was obtained from bark-exuded gum from another tree. The novel species was defined using molecular characteristics and subsequently characterized with respect to morphological, physiological, and biochemical properties. A neighbor-joining analysis using the sequences of the D1/D2 domains of the large subunit ribosomal RNA gene revealed that N. atacamensis clustered with Nakazawaea pomicola. The sequence of N. atacamensis differed from closely related species by 1.3%-5.2% in the D1/D2 domains. A phylogenomic analysis based on single-nucleotide polymorphism's data confirms that the novel species belongs to the genus Nakazawaea, where N. atacamensis clustered with N. peltata. Phenotypic comparisons demonstrated that N. atacamensis exhibited distinct carbon assimilation patterns compared to its related species. Genome sequencing of the strain ATA-11A-BT revealed a genome size of approximately 12.4 Mbp, similar to other Nakazawaea species, with 5116 protein-coding genes annotated using InterProScan. In addition, N. atacamensis exhibited the capacity to ferment synthetic wine must, representing a potential new yeast for mono or co-culture wine fermentations. This comprehensive study expands our understanding of the genus Nakazawaea and highlights the ecological and industrial potential of N. atacamensis in fermentation processes. The holotype of N. atacamensis sp. nov. is CBS 18375T . The Mycobank number is MB 849680.

Neurodegenerative Proteinopathies Induced by Environmental Pollutants: Heat Shock Proteins and Proteasome as Promising Therapeutic Tools.

Environmental pollutants' (EPs) amount and diversity have increased in recent years due to anthropogenic activity. Several neurodegenerative diseases (NDs) are theorized to be related to EPs, as their incidence has increased in a similar way to human EPs exposure and they reproduce the main ND hallmarks. EPs induce several neurotoxic effects, including accumulation and gradual deposition of misfolded toxic proteins, producing neuronal malfunction and cell death. Cells possess different mechanisms to eliminate these toxic proteins, including heat shock proteins (HSPs) and the proteasome system. The accumulation and deleterious effects of toxic proteins are induced through HSPs and disruption of proteasome proteins' homeostatic function by exposure to EPs. A therapeutic approach has been proposed to reduce accumulation of toxic proteins through treatment with recombinant HSPs/proteasome or the use of compounds that increase their expression or activity. Our aim is to review the current literature on NDs related to EP exposure and their relationship with the disruption of the proteasome system and HSPs, as well as to discuss the toxic effects of dysfunction of HSPs and proteasome and the contradictory effects described in the literature. Lastly, we cover the therapeutic use of developed drugs and recombinant proteasome/HSPs to eliminate toxic proteins and prevent/treat EP-induced neurodegeneration.

A 17.8-20.2 GHz Compact Vector-Sum Phase Shifter in 130 nm SiGe BiCMOS Technology for LEO Gateways Receivers.

This paper presents a novel and compact vector modulator (VM) architecture implemented in 130 nm SiGe BiCMOS technology. The design is suitable for use in receive phased arrays for the gateways of major low Earth orbit (LEO) constellations that operate in the 17.8 to 20.2 GHz frequency range. The proposed architecture uses four variable gain amplifiers (VGA) that are active at any given time and are switched to generate the four quadrants. Compared to conventional architectures, this structure is more compact and produces double the output amplitude. The design offers 6-bit phase control for 360°, and the total root mean square (RMS) phase and gain errors are 2.36° and 1.46 dB, respectively. The design occupies an area of 1309.4 µm × 1783.8 µm (including pads).

A Comparative Analysis of Doherty and Outphasing MMIC GaN Power Amplifiers for 5G Applications.

A comparison between a fully integrated Doherty power amplifier (DPA) and outphasing power amplifier (OPA) for fifth Generation (5G) wireless communications is presented in this paper. Both amplifiers are integrated using pHEMT transistors from the OMMIC's 100 nm GaN-on-Si technology (D01GH). After a theoretical analysis, the design and layout of both circuits are presented. The DPA uses an asymmetric configuration where the main amplifier is biased in class AB and the auxiliary amplifier is biased in class C, while the OPA uses two amplifiers biased in class B. In the comparative analysis, it has been observed that the OPA presents a better performance in terms of maximum power added efficiency (PAE), while the DPA provides higher linearity and efficiency at 7.5 dB output back-off (OBO). At a 1 dB compression point, the OPA exhibits an output power of 33 dBm with a maximum PAE of 58.3% compared to 44.2% for the DPA for an output power of 35 dBm, and at 7.5 dB OBO, the DPA achieves a PAE of 38.5%, while the OPA achieves 26.1%. The area has been optimized using absorbing adjacent component techniques, resulting in an area of 3.26 mm2 for the DPA and 3.18 mm2 for the OPA.

Dynamical Gauge Fields with Bosonic Codes.

The quantum simulation of dynamical gauge field theories offers the opportunity to study complex high-energy physics with controllable low-energy devices. For quantum computation, bosonic codes promise robust error correction that exploits multiparticle redundancy in bosons. Here, we demonstrate how bosonic codes can be used to simulate dynamical gauge fields. We encode both matter and dynamical gauge fields in a network of resonators that are coupled via three-wave mixing. The mapping to a Z_{2} dynamical lattice gauge theory is established when the gauge resonators operate as Schrödinger cat states. We explore the optimal conditions under which the system preserves the required gauge symmetries. Our findings promote realizing high-energy models using bosonic codes.

Cadmium-promoted thyroid hormones disruption mediates ROS, inflammation, Aß and Tau proteins production, gliosis, spongiosis and neurodegeneration in rat basal forebrain.

Cadmium (Cd) produces cognition decline following single and repeated treatment, although the complete mechanisms are still unrevealed. Basal forebrain (BF) cholinergic neurons innervate the cortex and hippocampus, regulating cognition. Cd single and repeated exposure induced BF cholinergic neuronal loss, partly through thyroid hormones (THs) disruption, which may cause the cognition decline observed following Cd exposure. However, the mechanisms through which THs disruption mediate this effect remain unknown. To research the possible mechanisms through which Cd-induced THs deficiency may mediate BF neurodegeneration, Wistar male rats were treated with Cd for 1- (1 mg/kg) or 28-days (0.1 mg/kg) with or without triiodothyronine (T3, 40 µg/kg/day). Cd exposure promoted neurodegeneration, spongiosis, gliosis and several mechanisms related to these alterations (increased H202, malondialdehyde, TNF-α, IL-1ß, IL-6, BACE1, Aß and phosphorylated-Tau levels, and decreased phosphorylated-AKT and phosphorylated-GSK-3ß levels). T3 supplementation partially reversed the effects observed. Our results show that Cd induces several mechanisms that may be responsible for the neurodegeneration, spongiosis and gliosis observed in the rats' BF, which are partially mediated by a reduction in THs levels. These data may help to explain the mechanisms through which Cd induces BF neurodegeneration, possibly leading to the cognitive decline observed, providing new therapeutic tools to prevent and treat these damages.

A 2-V 1.4-dB NF GaAs MMIC LNA for K-Band Applications.

A 1.4-dB Noise Figure (NF) four-stage K-band Monolithic Microwave Integrated Circuit (MMIC) Low-Noise Amplifier (LNA) in UMS 100 nm GaAs pHEMT technology is presented. The proposed circuit is designed to cover the 5G New Release n258 frequency band (24.25-27.58 GHz). Momentum EM post-layout simulations reveal the circuit achieves a minimum NF of 1.3 dB, a maximum gain of 34 dB, |S11| better than -10 dB from 23 GHz to 29 GHz, a P1dB of -18 dBm and an OIP3 of 24.5 dBm. The LNA draws a total current of 59.1 mA from a 2 V DC supply and results in a chip size of 3300 × 1800 µm2 including pads. We present a design methodology focused on the selection of the active device size and DC bias conditions to obtain the lowest NF when source degeneration is applied. The design procedure ensures a minimum NF design by selecting a device which facilitates a simple input matching network implementation and obtains a reasonable input return loss thanks to the application of source degeneration. With this approach the input matching network is implemented with a shunt stub and a transmission line, therefore minimizing the contribution to the NF achieved by the first stage. Comparisons with similar works demonstrate the developed circuit is very competitive with most of the state-of-the-art solutions.

Phased Array Antenna Analysis Workflow Applied to Gateways for LEO Satellite Communications.

Nowadays, mega-constellations of Low Earth Orbit (LEO) satellites have become increasingly important to provide high-performance Internet access with global coverage. This paper provides an updated comparison of four of the largest LEO mega-constellations: Telesat, SpaceX, OneWeb and Amazon. It describes the gateway design workflow from the patch antenna to phased array analysis. Patch antennas are developed for both transmission and reception after a thorough examination of the four systems. The results of electromagnetic simulation using Advanced Design Software (ADS) Momentum are shown, including their radiation pattern. Finally, a model of the gateway phased array using SystemVue is obtained using hexagonal, circular, and square arrays. According to the required effective isotropic radiated power (EIRP) and gain, the antenna sizes for the four constellations are estimated. As an example, for SpaceX constellation, a reception antenna with 8910 radiating elements using a hexagonal distribution with a gain of 46.9 dB and a sensitivity of -113.1 dBm was obtained.

Insulin Signaling Disruption and INF-γ Upregulation Induce Aß1-42 and Hyperphosphorylated-Tau Proteins Synthesis and Cell Death after Paraquat Treatment of Primary Hippocampal Cells.

Acute and long-term paraquat (PQ) exposure produces hippocampal neurodegeneration and cognition decline. Although some mechanisms involved in these effects were found, the rest are unknown. PQ treatment, for 1 and 14 days, upregulated interferon-gamma signaling, which reduced insulin levels and downregulated the insulin pathway through phosphorylated-c-Jun N-terminal-kinase upregulation, increasing glucose levels and the production of Aß1-42 and phosphorylated-tau, by beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) overexpression and phosphorylated-GSK3ß (p-GSK3ß; ser9) level reduction, respectively, which induced primary hippocampal neuronal loss. This novel information on the PQ mechanisms leading to hippocampal neurodegeneration could help reveal the PQ actions that lead to cognition dysfunction.

Miniature Wide-Band Noise-Canceling CMOS LNA.

In this paper, a wide-band noise-canceling (NC) current conveyor (CC)-based CMOS low-noise amplifier (LNA) is presented. The circuit employs a CC-based approach to obtain wide-band input matching without the need for bulky inductances, allowing broadband performance with a very small area used. The NC technique is applied by subtracting the input transistor's noise contribution to the output and achieves a noise figure (NF) reduction from 4.8 dB to 3.2 dB. The NC LNA is implemented in a UMC 65-nm CMOS process and occupies an area of only 160 × 80 µm2. It achieves a stable frequency response from 0 to 6.2 GHz, a maximum gain of 15.3 dB, an input return loss (S11) < −10 dB, and a remarkable IIP3 of 7.6 dBm, while consuming 18.6 mW from a ±1.2 V DC supply. Comparisons with similar works prove the effectiveness of this new implementation, showing that the circuit obtains a noteworthy performance trade-off.

Non-Hermitian chiral phononics through optomechanically induced squeezing.

Imposing chirality on a physical system engenders unconventional energy flow and responses, such as the Aharonov-Bohm effect1 and the topological quantum Hall phase for electrons in a symmetry-breaking magnetic field. Recently, great interest has arisen in combining that principle with broken Hermiticity to explore novel topological phases and applications2-16. Here we report phononic states with unique symmetries and dynamics that are formed when combining the controlled breaking of time-reversal symmetry with non-Hermitian dynamics. Both of these are induced through time-modulated radiation pressure forces in small nano-optomechanical networks. We observe chiral energy flow among mechanical resonators in a synthetic dimension and Aharonov-Bohm tuning of their eigenmodes. Introducing particle-non-conserving squeezing interactions, we observe a non-Hermitian Aharonov-Bohm effect in ring-shaped networks in which mechanical quasiparticles experience parametric gain. The resulting complex mode spectra indicate flux-tuning of squeezing, exceptional points, instabilities and unidirectional phononic amplification. This rich phenomenology points the way to exploring new non-Hermitian topological bosonic phases and applications in sensing and transport that exploit spatiotemporal symmetry breaking.

Area-Efficient Integrated Current-Reuse Feedback Amplifier for Wake-Up Receivers in Wireless Sensor Network Applications.

Wireless sensor network (WSN) applications are under extensive research and development due to the need to interconnect devices with each other. To reduce latency while keeping very low power consumption, the implementation of a wake-up receiver (WuR) is of particular interest. In WuR implementations, meeting high performance metrics is a design challenge, and the obtention of high-sensitivity, high data rate, low-power-consumption WuRs is not a straightforward procedure. The focus of our proposals is centered on power consumption and area reduction to provide high integrability and maintain a low cost-per-node, while we simultaneously improve circuit sensitivity. Firstly, we present a two-stage design based on a feedback technique and improve the area use, power consumption and sensitivity of the circuit by adding a current-reuse approach. The first solution is composed of a feedback amplifier, two op-amps plus a low-pass filter. The circuit achieves a sensitivity of -63.2 dBm with a power consumption of 6.77 µA and an area as low as 398 × 266 µm2. With the current-reuse feedback amplifier, the power consumption is halved in the second circuit (resulting in 3.63 µA), and the resulting circuit area is as low as 262 × 262 µm2. Thanks to the nature of the circuit, the sensitivity is improved to -75 dBm. This latter proposal is particularly suitable in applications where a fully integrated WuR is desired, providing a reasonable sensitivity with a low power consumption and a very low die footprint, therefore facilitating integration with other components of the WSN node. A thorough discussion of the most relevant state-of-the-art solutions is presented, too, and the two developed solutions are compared to the most relevant contributions available in the literature.

Cadmium-induced neurotoxic effects on rat basal forebrain cholinergic system through thyroid hormones disruption.

Cadmium (Cd) single and repeated exposure produces cognitive dysfunctions. Basal forebrain cholinergic neurons (BFCN) regulate cognitive functions. BFCN loss or cholinergic neurotransmission dysfunction leads to cognitive disabilities. Thyroid hormones (THs) maintain BFCN viability and functions, and Cd disrupts their levels. However, Cd-induced BFCN damages and THs disruption involvement was not studied. To research this we treated male Wistar rats intraperitoneally with Cd once (1 mg/kg) or repetitively for 28 days (0.1 mg/kg) with/without triiodothyronine (T3, 40 µg/kg/day). Cd increased thyroid-stimulating-hormone (TSH) and decreased T3 and tetraiodothyronine (T4). Cd altered cholinergic transmission and induced a more pronounced neurodegeneration on BFCN, mediated partially by THs reduction. Additionally, Cd antagonized muscarinic 1 receptor (M1R), overexpressed acetylcholinesterase S variant (AChE-S), downregulated AChE-R, M2R, M3R and M4R, and reduced AChE and choline acetyltransferase activities through THs disruption. These results may assist to discover cadmium mechanisms that induce cognitive disabilities, revealing a new possible therapeutic tool.

Bisphenol A single and repeated treatment increases HDAC2, leading to cholinergic neurotransmission dysfunction and SN56 cholinergic apoptotic cell death through AChE variants overexpression and NGF/TrkA/P75NTR signaling disruption.

Bisphenol-A (BPA), a widely used plasticizer, induces cognitive dysfunctions following single and repeated exposure. Several studies, developed in hippocampus and cortex, tried to find the mechanisms that trigger and mediate these dysfunctions, but those are still not well known. Basal forebrain cholinergic neurons (BFCN) innervate hippocampus and cortex, regulating cognitive function, and their loss or the induction of cholinergic neurotransmission dysfunction leads to cognitive disabilities. However, no studies were performed in BFCN. We treated wild type or histone deacetylase (HDAC2), P75NTR or acetylcholinesterase (AChE) silenced SN56 cholinergic cells from BF with BPA (0.001 µM-100 µM) with or without recombinant nerve growth factor (NGF) and with or without acetylcholine (ACh) for one- and fourteen days in order to elucidate the mechanisms underlying these effects. BPA induced cholinergic neurotransmission disruption through reduction of ChAT activity, and produced apoptotic cell death, mediated partially through AChE-S overexpression and NGF/TrkA/P75NTR signaling dysfunction, independently of cholinergic neurotransmission disruption, following one- and fourteen days of treatment. BPA mediates these alterations, in part, through HDAC2 overexpression. These data are relevant since they may help to elucidate the neurotoxic mechanisms that trigger the cognitive disabilities induced by BPA exposure, providing a new therapeutic approach.

Neuroprotective Action of Multitarget 7-Aminophenanthridin-6(5H)-one Derivatives against Metal-Induced Cell Death and Oxidative Stress in SN56 Cells.

Neurodegenerative diseases have been associated with brain metal accumulation, which produces oxidative stress (OS), matrix metalloproteinases (MMPs) induction, and neuronal cell death. Several metals have been reported to downregulate both the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway and the antioxidant enzymes regulated by it, mediating OS induction and neurodegeneration. Among a recently discovered family of multitarget 7-amino-phenanthridin-6-one derivatives (APH) the most promising compounds were tested against metal-induced cell death and OS in SN56 cells. These compounds, designed to have chelating activity, are known to inhibit some MMPs and to present antioxidant and neuroprotective effects against hydrogen peroxide treatment to SN56 neuronal cells. However, the mechanisms that mediate this protective effect are not fully understood. The obtained results show that compounds APH1, APH2, APH3, APH4, and APH5 were only able to chelate iron and copper ions among all metals studied and that APH3, APH4, and APH5 were also able to chelate mercury ion. However, none of them was able to chelate zinc, cadmium, and aluminum, thus exhibiting selective chelating activity that can be partly responsible for their neuroprotective action. Otherwise, our results indicate that their antioxidant effect is mediated through induction of the Nrf2 pathway that leads to overexpression of antioxidant enzymes. Finally, these compounds exhibited neuroprotective effects, reversing partially or completely the cytotoxic effects induced by the metals studied depending on the compound used. APH4 was the most effective and safe compound.

Aryl Hydrocarbon Receptor Activation Produces Heat Shock Protein 90 and 70 Overexpression, Prostaglandin E2/Wnt/ß-Catenin Signaling Disruption, and Cell Proliferation in MCF-7 and MDA-MB-231 Cells after 24 h and 14 Days of Chlorpyrifos Treatment.

The biocide chlorpyrifos (CPF) was described to increase breast cancer risk in humans, to produce breast cancer in animals, and to induce cell proliferation in MCF-7 and MDA-MB-231 cells after 1 and 14 days of treatment. The entire mechanisms related to these CPF actions remain unknown. CPF induced cell proliferation in MCF-7 and MDA-MB-231 cells after 1 and 14 days of treatment by AhR activation through the PGE2/Wnt/ß-catenin pathway and HSP90 and HSP70 overexpression. Our results reveal new information on CPF toxic mechanisms induced in human breast cancer cell lines, which could assist in elucidating its involvement in breast cancer.

Chlorpyrifos induces cell proliferation in MCF-7 and MDA-MB-231 cells, through cholinergic and Wnt/ß-catenin signaling disruption, AChE-R upregulation and oxidative stress generation after single and repeated treatment.

Chlorpyrifos (CPF) biocide, is associated with breast cancer. The processes underlying this association have not been elucidated to date. CPF increases MCF-7 and MDA-MB-231 cell proliferation after acute and long-term treatment, partially through KIAA1363 overexpression and aryl-hydrocarbon receptor activation but also through estrogen receptor-alpha activation after 24 h exposure in MCF-7 cells, suggesting other mechanisms may be involved. CPF induces reactive oxygen species (ROS) generation, acetylcholine accumulation, and overexpression of acetylcholinesterase-R/S (AChE-R/S) variants, while it also alters the Wnt/ß-catenin pathway, both in vitro and in vivo, in processes different from cancer. These latter mechanisms are also linked to cell proliferation and could mediate this effect induced by CPF. Our results show that CPF (0.01-100 µM), following one-day and fourteen-days treatment, respectively, induced ROS generation and lipid peroxidation, and acetylcholine accumulation due to AChE inhibition, Wnt/ß-catenin up- or downregulation depending on the CPF treatment concentration, and AChE-R and AChE-S overexpression, with the latter being mediated through GSK-3ß activity alteration. Finally, CPF promoted cell division through ACh and ROS accumulation, AChE-R overexpression, and Wnt/ß-catenin signaling disruption. Our results provide novel information on the effect of CPF on human breast cancer cell lines that may help to explain its involvement in breast cancer.