Switchable and tunable terahertz metamaterial absorber with broadband and multi-band absorption.

In this paper, we propose and demonstrate a switchable terahertz metamaterial absorber with broadband and multi-band absorption based on a simple configuration of graphene and vanadium dioxide (VO2). The switchable functional characteristics of the absorber can be achieved by changing the phase transition property of VO2. When VO2 is insulating, the device acts as a broadband absorber with absorbance greater than 90% under normal incidence from 1.06 THz to 2.58 THz. The broadband absorber exhibits excellent absorption performance under a wide range of incident and polarization angles for TE and TM polarizations. Moreover, the absorption bandwidth and intensity of the absorber can be dynamically adjusted by changing the Fermi energy level of graphene. When VO2 is in the conducting state, the designed metamaterial device acts as a multi-band absorber with absorption frequencies at 1 THz, 2.45 THz, and 2.82 THz. The multi-band absorption is achieved owing to the fundamental resonant modes of the graphene ring sheet, VO2 hollow ring patch, and coupling interaction between them. Moreover, the multi-band absorber is insensitive to polarization and incident angles for TE and TM polarizations, and the three resonance frequencies can be reconfigured by changing the Fermi energy level of graphene. Our designed device exhibits the merits of bi-functionality and a simple configuration, which is very attractive for potential terahertz applications such as intelligent attenuators, reflectors, and spatial modulators.

Urate mitigates oxidative stress and motor neuron toxicity of astrocytes derived from ALS-linked SOD1G93A mutant mice.

Dominant mutations in an antioxidant enzyme superoxide dismutase-1 (SOD1) cause amyotrophic lateral sclerosis (ALS), an adult-onset neurodegenerative disease characterized by loss of motor neurons. Oxidative stress has also been linked to many of the neurodegenerative diseases and is likely a central mechanism of motor neuron death in ALS. Astrocytes derived from mutant SOD1G93A mouse models or patients play a significant role in the degeneration of spinal motor neurons in ALS through a non-cell-autonomous process. Here we characterize the neuroprotective effects and mechanisms of urate (a.k.a. uric acid), a major endogenous antioxidant and a biomarker of favorable ALS progression rates, in a cellular model of ALS. Our results demonstrate a significant protective effect of urate against motor neuron injury evoked by mutant astrocytes derived from SOD1G93A mice or hydrogen peroxide induced oxidative stress. Overall, these results implicate astrocyte dependent protective effect of urate in a cellular model of ALS. These findings together with our biomarker data may advance novel targets for treating motor neuron disease.

Disrupted and transgenic urate oxidase alter urate and dopaminergic neurodegeneration.

Urate is the end product of purine metabolism in humans, owing to the evolutionary disruption of the gene encoding urate oxidase (UOx). Elevated urate can cause gout and urolithiasis and is associated with cardiovascular and other diseases. However, urate also possesses antioxidant and neuroprotective properties. Recent convergence of epidemiological and clinical data has identified urate as a predictor of both reduced risk and favorable progression of Parkinson's disease (PD). In rodents, functional UOx catalyzes urate oxidation to allantoin. We found that UOx KO mice with a constitutive mutation of the gene have increased concentrations of brain urate. By contrast, UOx transgenic (Tg) mice overexpressing the enzyme have reduced brain urate concentrations. Effects of the complementary UOx manipulations were assessed in a mouse intrastriatal 6-hydroxydopamine (6-OHDA) model of hemiparkinsonism. UOx KO mice exhibit attenuated toxic effects of 6-OHDA on nigral dopaminergic cell counts, striatal dopamine content, and rotational behavior. Conversely, Tg overexpression of UOx exacerbates these morphological, neurochemical, and functional lesions of the dopaminergic nigrostriatal pathway. Together our data support a neuroprotective role of endogenous urate in dopaminergic neurons and strengthen the rationale for developing urate-elevating strategies as potential disease-modifying therapy for PD.

Neuroprotective effects of urate are mediated by augmenting astrocytic glutathione synthesis and release.

Urate has emerged as a promising target for neuroprotection based on epidemiological observations, preclinical models, and early clinical trial results in multiple neurologic diseases, including Parkinson's disease (PD). This study investigates the astrocytic mechanism of urate's neuroprotective effect. Targeted biochemical screens of conditioned medium from urate- versus vehicle-treated astrocytes identified markedly elevated glutathione (GSH) concentrations as a candidate mediator of urate's astrocyte-dependent neuroprotective effects. Urate treatment also induced the nuclear translocation of the nuclear factor (erythroid-derived 2)-like 2 (Nrf2) protein and transcriptional activation of its key target genes in primary astrocytic cultures. Urate's neuroprotective effect was attenuated when GSH was depleted in the conditioned media either by targeting its synthesis or release by astrocytes. Overall, these results implicate GSH as the extracellular astrocytic factor mediating the protective effect of urate in a cellular model of PD. These results also show that urate can employ a novel indirect neuroprotective mechanism via induction of the Nrf2 signaling pathway, a master regulator of the response to oxidative stress, in astrocytes.

UAV-based modelling of vegetation recovery under extreme habitat stresses in the water level fluctuation zone of the Three Gorges Reservoir, China.

Impoundment of the Three Gorges Reservoir on the upper Yangtze River has remarkably altered hydrological regime within the dammed reaches, triggering structural and functional changes of the riparian ecosystem. Up to date, how vegetation recovers in response to compound habitat stresses in the water level fluctuation zone remains inexplicitly understood. In this study, plant above-ground biomass (AGB) in a selected water level fluctuation zone was quantified to depict its spatial and temporal pattern using unmanned aerial vehicle (UAV)-derived multispectral images and screened empirical models. The contributions of multiple habitat stressors in governing vegetation recovery dynamics along the environmental gradient were further explored. Screened random forest models indicated relatively higher accuracy in AGB estimation, with R2 being 0.68, 0.79 and 0.62 during the sprouting, growth, and mature periods, respectively. AGB displayed a significant linear increasing trend along the elevational gradient during the sprouting and early growth period, while it showed an inverted U-shaped pattern during late growth and mature period. Flooding duration, magnitude and timing were found to exert greater negative effects on plant sprouting and biomass accumulation and acted as decisive factors in governing the elevation-dependent pattern of AGB. Localized spatial variations in AGB were modulated by other stressors such as sediment burial, soil erosion, soil moisture and nutrient content. Occurrence of episodic summer floods and vegetation distribution were responsible for an inverted U-shaped pattern of AGB during the late growth and mature period. Generally, AGB reached its peak in August, thereafter an obvious decline by an unprecedent dry-hot climatic event. The water level fluctuations with cumulative flooding effects exerted substantial control on AGB temporal dynamics, while climatic condition played a secondary role. Herein, further restorative efforts need to be directed to screening suitable species, maintaining favorable soil condition, and improving vegetation pattern to balance the many trade-offs.

Prenatal nicotine exposure mouse model showing hyperactivity, reduced cingulate cortex volume, reduced dopamine turnover, and responsiveness to oral methylphenidate treatment.

Cigarette smoking, nicotine replacement therapy, and smokeless tobacco use during pregnancy are associated with cognitive disabilities later in life in children exposed prenatally to nicotine. The disabilities include attention deficit hyperactivity disorder (ADHD) and conduct disorder. However, the structural and neurochemical bases of these cognitive deficits remain unclear. Using a mouse model we show that prenatal nicotine exposure produces hyperactivity, selective decreases in cingulate cortical volume, and radial thickness, as well as decreased dopamine turnover in the frontal cortex. The hyperactivity occurs in both male and female offspring and peaks during the "active" or dark phase of the light/dark cycle. These features of the mouse model closely parallel the human ADHD phenotype, whether or not the ADHD is associated with prenatal nicotine exposure. A single oral, but not intraperitoneal, administration of a therapeutic equivalent dose (0.75 mg/kg) of methylphenidate decreases the hyperactivity and increases the dopamine turnover in the frontal cortex of the prenatally nicotine exposed mice, once again paralleling the therapeutic effects of this compound in ADHD subjects. Collectively, our data suggest that the prenatal nicotine exposure mouse model has striking parallels to the ADHD phenotype not only in behavioral, neuroanatomical, and neurochemical features, but also with respect to responsiveness of the behavioral phenotype to methylphenidate treatment. The behavioral, neurochemical, and anatomical biomarkers in the mouse model could be valuable for evaluating new therapies for ADHD and mechanistic investigations into its etiology.

Peripheral MC1R activation modulates immune responses and is neuroprotective in a mouse model of Parkinson's disease.

Background: Melanocortin 1 receptor (MC1R) is a key pigmentation gene, and loss-of-function of MC1R variants that produce red hair may be associated with Parkinson's disease (PD). We previously reported compromised dopaminergic neuron survival in Mc1r mutant mice and dopaminergic neuroprotective effects of local injection of a MC1R agonist to the brain or a systemically administered MC1R agonist with appreciable CNS permeability. Beyond melanocytes and dopaminergic neurons, MC1R is expressed in other peripheral tissues and cell types, including immune cells. The present study investigates the impact of NDP-MSH, a synthetic melanocortin receptor (MCR) agonist that does not cross BBB, on the immune system and the nigrostriatal dopaminergic system in mouse model of PD. Methods: C57BL/6 mice were treated systemically with MPTP.HCl (20 mg/kg) and LPS (1 mg/kg) from day 1 to day 4 and NDP-MSH (400 µg/kg) or vehicle from day 1 to day 12 following which the mice were sacrificed. Peripheral and CNS immune cells were phenotyped and inflammatory markers were measured. The nigrostriatal dopaminergic system was assessed behaviorally, chemically, immunologically, and pathologically. To understand the role of regulatory T cells (Tregs) in this model, CD25 monoclonal antibody was used to deplete CD25+ Tregs. Results: Systemic NDP-MSH administration significantly attenuated striatal dopamine depletion and nigral dopaminergic neuron loss induced by MPTP+LPS. It improved the behavioral outcomes in the pole test. Mc1r mutant mice injected with NDP-MSH in the MPTP and LPS paradigm showed no changes in striatal dopamine levels suggesting that the NDP-MSH acts through the MC1R pathway. Although no NDP-MSH was detected in the brain, peripheral, NDP-MSH attenuated neuroinflammation as observed by diminished microglial activation in the nigral region, along with reduced TNF-α and IL1ß levels in the ventral midbrain. Depletion of Tregs limited the neuroprotective effects of NDP-MSH. Conclusions: Our study demonstrates that peripherally acting NDP-MSH confers protection on dopaminergic nigrostriatal neurons and reduces hyperactivated microglia. NDP-MSH modulates peripheral immune responses, and Tregs may be involved in the neuroprotective effect of NDP-MSH.

Microglia-dependent neuroprotective effects of 4-octyl itaconate against rotenone-and MPP+-induced neurotoxicity in Parkinson's disease.

Chronic neuroinflammation is implicated in the pathogenesis of Parkinson's disease (PD), one of the most common neurodegenerative diseases. Itaconate, an endogenous metabolite derived from the tricarboxylic acid cycle via immune-responsive gene 1 activity, may mediate anti-inflammatory responses by activation of the nuclear factor erythroid 2-related factor 2 (Nrf2) antioxidant pathway. This study investigates the neuroprotective potential of 4-octyl itaconate (OI), a cell-permeable derivative of itaconate, in cellular models of PD. OI not only suppressed lipopolysaccharide-induced proinflammatory cascades of inducible nitric oxide synthase, cyclooxygenase-2, and cytokines release in mouse BV2 microglial cells but also activated the Nrf2 signaling pathway and its downstream targets in these cells. Conditioned medium derived from OI-treated BV2 cells protected against rotenone- and MPP+-induced neurotoxicity in Neuro 2A cells. Overall, our findings support the anti-inflammatory neuroprotective potential of OI in PD.

Peripheral MC1R Activation Modulates Immune Responses and is Neuroprotective in a Mouse Model of Parkinson's Disease.

BACKGROUND: Melanocortin 1 receptor (MC1R) is a key pigmentation gene, and loss-of-function of MC1R variants that produce red hair may be associated with Parkinson's disease (PD). We previously reported compromised dopaminergic neuron survival in Mc1r mutant mice and dopaminergic neuroprotective effects of local injection of a MC1R agonist to the brain or a systemically administered MC1R agonist with appreciable central nervous system (CNS) permeability. Beyond melanocytes and dopaminergic neurons, MC1R is expressed in other peripheral tissues and cell types, including immune cells. The present study investigates the impact of NDP-MSH, a synthetic melanocortin receptor (MCR) agonist that does not cross BBB, on the immune system and the nigrostriatal dopaminergic system in mouse model of PD. METHODS: C57BL/6 mice were treated systemically with MPTP.HCl (20 mg/kg) and LPS (1 mg/kg) from day 1 to day 4 and NDP-MSH (400 µg/kg) or vehicle from day 1 to day 12 following which the mice were sacrificed. Peripheral and CNS immune cells were phenotyped and inflammatory markers were measured. The nigrostriatal dopaminergic system was assessed behaviorally, chemically, immunologically, and pathologically. To understand the role of regulatory T cells (Tregs) in this model, CD25 monoclonal antibody was used to deplete CD25 + Tregs. RESULTS: Systemic NDP-MSH administration significantly attenuated striatal dopamine depletion and nigral dopaminergic neuron loss induced by MPTP + LPS. It improved the behavioral outcomes in the pole test. Mc1r mutant mice injected with NDP-MSH in the MPTP and LPS paradigm showed no changes in striatal dopamine levels suggesting that the NDP-MSH acts through the MC1R pathway. Although no NDP-MSH was detected in the brain, peripheral, NDP-MSH attenuated neuroinflammation as observed by diminished microglial activation in the nigral region, along with reduced TNF-α and IL1ß levels in the ventral midbrain. Depletion of Tregs was associated with diminished neuroprotective effects of NDP-MSH. CONCLUSIONS: Our study demonstrates that peripherally acting NDP-MSH confers protection on dopaminergic nigrostriatal neurons and reduces hyperactivated microglia. NDP-MSH modulates peripheral immune responses, and Tregs may be involved in the neuroprotective effect of NDP-MSH.

Estimated prevalence and sociodemographic correlates of mental disorders in medical students of Hebei Province, China: A cross-sectional study.

BACKGROUND: In China, the identification rate and treatment rate of mental disorders are low, and there are few surveys on the prevalence of mental disorders among college students using diagnostic tools such as Mini-International Neuropsychiatric Interview (MINI), so the prevalence and treatment of mental disorders among college students are unclear. AIM: To estimate prevalence of mental disorders among medical students in Hebei Province, and provide guidance for improving their mental health. METHODS: This was a cross-sectional study based on an Internet-based survey. Three levels of medical students in Hebei Province were randomly selected (by cluster sampling) for screening. Using the information network assessment system, the subjects scanned the 2D code with their mobile phones, clicked to sign the informed consent, and answered a scale. A self-designed general status questionnaire was used to collect information about age, gender, ethnicity, grade, and origin of students. The MINI 5.0. was used to investigate mental disorders. Data analysis was performed with SPSS software. Statistically significant findings were determined using a two-tailed P value of 0.05. RESULTS: A total of 7117 subjects completed the survey between October 11 and November 7, 2021. The estimated prevalence of any mental disorders within 12 mo was 7.4%. Mood disorders were the most common category (4.3%), followed by anxiety disorders (3.9%); 15.0% had been to psychological counseling, while only 5.7% had been to a psychiatric consultation, and only 10% had received drug therapy in the past 12 mo. CONCLUSION: Although the estimated prevalence of mental disorders in medical students is lower than in the general population, the rate of adequate treatment is low. We determined that improving the mental health of medical students is an urgent matter.

Protection of dopaminergic cells by urate requires its accumulation in astrocytes.

Urate is the end product of purine metabolism and a major antioxidant circulating in humans. Recent data link higher levels of urate with a reduced risk of developing Parkinson's disease and with a slower rate of its progression. In this study, we investigated the role of astrocytes in urate-induced protection of dopaminergic cells in a cellular model of Parkinson's disease. In mixed cultures of dopaminergic cells and astrocytes oxidative stress-induced cell death and protein damage were reduced by urate. By contrast, urate was not protective in pure dopaminergic cell cultures. Physical contact between dopaminergic cells and astrocytes was not required for astrocyte-dependent rescue as shown by conditioned medium experiments. Urate accumulation in dopaminergic cells and astrocytes was blocked by pharmacological inhibitors of urate transporters expressed differentially in these cells. The ability of a urate transport blocker to prevent urate accumulation into astroglial (but not dopaminergic) cells predicted its ability to prevent dopaminergic cell death. Transgenic expression of uricase reduced urate accumulation in astrocytes and attenuated the protective influence of urate on dopaminergic cells. These data indicate that urate might act within astrocytes to trigger release of molecule(s) that are protective for dopaminergic cells.

C-Band 30 W High PAE Power Amplifier MMIC with Second Harmonic Suppression for Radar Network Application.

In order to meet the application requirements of radar networks for high efficiency and high second harmonic suppression (SHS) of power amplifiers, this paper proposes a C-band 30 W power amplifier (PA) microwave monolithic integrated circuit (MMIC) based on 0.25 µm gallium nitride (GaN) high electron mobility transistor (HEMT) process. The proposed PA uses a two-stage amplifier structure to achieve high power gain. A topology with SHS is designed in the output-matching network. Besides, the large signal model load pull simulation and the harmonic control technology in the output stage are used to improve efficiency. The high-power additional efficiency (PAE) and high SHS of the PA MMIC are achieved simultaneously. In the 5-6 GHz frequency range, multiple indicator measurements of the proposed PA show that output power is over 45 dBm, the PAE is more than 57%, the SHS exceeds 45 dBc, the power gain is greater than 24 dB, which are conducted under the condition of 100 µs pulse width and 10% duty cycle. In addition, the size of the PA MMIC, including bonding pads, is 3.3 × 3.1 mm2.

A Fast and Label-Free Potentiometric Method for Direct Detection of Glutamine with Silicon Nanowire Biosensors.

In this paper, a potentiometric method is used for monitoring the concentration of glutamine in the bioprocess by employing silicon nanowire biosensors. Just one hydrolyzation reaction was used, which is much more convenient compared with the two-stage reactions in the published papers. For the silicon nanowire biosensor, the Al2O3 sensing layer provides a highly sensitive to solution-pH, which has near-Nernstian sensitivity. The sensitive region to detect glutamine is from ≤40 µM to 20 mM. The Sigmoidal function was used to model the pH-signal variation versus the glutamine concentration. Compared with the amperometric methods, a consistent result from different devices could be directly obtained. It is a fast and direct method achieved with our real-time setup. Also, it is a label-free method because just the pH variation of the solution is monitored. The obtained results show the feasibility of the potentiometric method for monitoring the glutamine concentrations in fermentation processes. Our approach in this paper can be applied to various analytes.

Melanocortin 1 receptor activation protects against alpha-synuclein pathologies in models of Parkinson's disease.

BACKGROUND: Epidemiological studies suggest a link between the melanoma-related pigmentation gene melanocortin 1 receptor (MC1R) and risk of Parkinson's disease (PD). We previously showed that MC1R signaling can facilitate nigrostriatal dopaminergic neuron survival. The present study investigates the neuroprotective potential of MC1R against neurotoxicity induced by alpha-synuclein (αSyn), a key player in PD genetics and pathogenesis. METHODS: Nigral dopaminergic neuron toxicity induced by local overexpression of aSyn was assessed in mice that have an inactivating mutation of MC1R, overexpress its wild-type transgene, or were treated with MC1R agonists. The role of nuclear factor erythroid 2-related factor 2 (Nrf2) in MC1R-mediated protection against αSyn was characterized in vitro. Furthermore, MC1R expression was determined in human postmortem midbrain from patients with PD and unaffected subjects. RESULTS: Targeted expression of αSyn in the nigrostriatal pathway induced exacerbated synuclein pathologies in MC1R mutant mice, which were accompanied by neuroinflammation and altered Nrf2 responses, and reversed by the human MC1R transgene. Two MC1R agonists were neuroprotective against αSyn-induced dopaminergic neurotoxicity. In vitro experiments showed that Nrf2 was a necessary mediator of MC1R effects. Lastly, MC1R was present in dopaminergic neurons in the human substantia nigra and appeared to be reduced at the tissue level in PD patients. CONCLUSION: Our study supports an interaction between MC1R and αSyn that can be mediated by neuronal MC1R possibly through Nrf2. It provides evidence for MC1R as a therapeutic target and a rationale for development of MC1R-activating strategies for PD.

S- to X-Band Stretchable Inductors and Filters for Gigahertz Soft and Epidermal Electronics.

To fulfill the increasing demand for radiofrequency (RF) wireless communication capacity for epidermal electronics, stretchable integrated circuits (ICs) in the gigahertz (GHz) range are desirable. Lumped RF inductors, as a key component in RFICs, typically dominate a large portion of the circuit/chip area and therefore make such inductors mechanically stretchable is critical for GHz-frequency stretchable RFICs. Most of the reported stretchable inductors operate in the MHz frequency range. The only GHz stretchable inductor shows a quality factor of about 2, limiting its potential RF applications. Here, stretchable inductors with a high quality factor of Q > 12.6 and resonance operation frequency of fres > 11.6 GHz are demonstrated by combining microspirals with stretchable structures, overcoming all of the shortcomings of previous demonstrations. Furthermore, a stretchable 1.5-2.6 GHz filter with a peak insertion loss of -2.3 dB at 1.8 GHz is developed, showing negligible performance changes under stretching or on the skin to demonstrate the utility in practical wireless applications like GSM and Bluetooth (2.45 GHz) bands. The demonstrations can facilitate multiple GHz epidermal RFICs in the future.

High-Temperature-Annealed Flexible Carbon Nanotube Network Transistors for High-Frequency Wearable Wireless Electronics.

Semiconducting single-walled carbon nanotubes (SWNTs) are potential active materials for fast-growing flexible/wearable applications with low-power dissipation, especially suitable for increasingly important radio-frequency (RF) wireless biosensor systems. However, the operation frequency of the existing flexible carbon nanotube field-effect transistors (CNT-FETs) is far below the current state-of-the-art GSM spectrum frequency band (typical 850 MHz) for near-field wireless communication applications. In this paper, we successfully conduct a 900 °C annealing process for the flexible CNT-FETs and hence significantly improve their operation frequency up to 2.1 gigahertz (GHz), making it possible to cover the current GSM spectra for integrated wireless sensor systems. The high-temperature annealing process significantly improves the electrical characteristic of the flexible CNT-FETs by removing the surfactant impurities of the SWNT materials. The obtained flexible CNT-FETs exhibit record transconductance (gm) as high as 48 µS/µm. Despite an applied strain level of 2%, a characteristic frequency of over 1 GHz is observed. Further demonstration of GHz performance is also exhibited for flexible RF integrated circuits (ICs) such as frequency multipliers and mixers, which are the fundamental components for wireless applications. This work offers a new pathway for realizing SWNT-based wearable wireless GHz sensor systems with power efficiency.

A 135-190 GHz Broadband Self-Biased Frequency Doubler using Four-Anode Schottky Diodes.

This paper describes the design and demonstration of a 135-190 GHz self-biased broadband frequency doubler based on planar Schottky diodes. Unlike traditional bias schemes, the diodes are biased in resistive mode by a self-bias resistor; thus, no additional bias voltage is needed for the doubler. The Schottky diodes in this verification are micron-scaled devices with an anode area of 6.6 µm2 and an epitaxial layer thickness of 0.26 µm. For accurate design of the doubler, the 3D-EM model of the Schottky diode is built up to extract the parasitic parameters induced by the diode package when frequency rises up to the terahertz band. In order to implement broadband working, input waveguide steps, output suspended microstrip steps, and output probe with bias filter are all used as matching elements for impedance matching. Measured results show that the doubler exhibits a 3 dB bandwidth of 34% from 135 GHz to 190 GHz, with a conversion efficiency of above 4% when supplied with 100 mW of input power. A 17.8 mW peak output power with a 10.2% efficiency was measured at 166 GHz when the input power was 174 mW. The measured results agree well with the simulated results, which indicates that the self-bias scheme for Schottky diode-based frequency multipliers is feasible and effective.

Investigation on the I⁻V Kink Effect in Large Signal Modeling of AlGaN/GaN HEMTs.

The effect brought by the I⁻V kink effect on large signal performance of AlGaN/GaN high electron mobility transistors (HEMTs) was investigated in this paper. An improved compact model was proposed to accurately characterize the I⁻V kink effect. The bias dependence of the I⁻V kink effect has also been taken into consideration. AlGaN/GaN HEMTs with different gate width were utilized to validate the proposed model. Built on the proposed model, the effect brought by the I⁻V kink effect on large signal performance has been studied. Results show that the I⁻V kink effect will lead to the degradation of characteristics, including output power, gain, and power-added efficiency at the saturation region. Furthermore, the influence of the I⁻V kink effect was found to be related with the input power and the static bias point in this work. The time domain waveform and AC dynamic load line were used for validation of results based on simulation. The consequences of this paper will be useful for the optimization of practical circuit design.

Bending Limit Tests for Ultra-Thin Liquid Crystal Polymer Substrate Based on Flexible Microwave Components.

In this paper, bending limit tests for one ultra-thin liquid crystal polymer (LCP) substrate (Rogers 3850) based on the mechanical properties of flexible microwave microstrip components are presented. First, a set of 50 Ω microstrip lines, a band-pass filter, and a stepped impedance filter in X-band, are designed by using double clapped LCPs with 50 µm thickness of substrate and 18 µm thickness of copper, which is fabricated by conventional photolithography. Then, the limit tests of the flexibility of the LCP microwave microstrip components are presented, and the range of the bending limit radius, from 1 mm to 0.75 mm, is demonstrated from the testing results. It is found that the cause for component failure is fracture of the copper (18 µm thickness) laminate, according to the bending limit test experiments. Finally, the analysis of the reasons for the collapse of the microwave components, under bending situations, is explored. The results from this work would be useful for further designs of the flexible microwave devices and systems on LCP substrates, with compact sizes and good performance.

Frequency Tuning of Graphene Nanoelectromechanical Resonators via Electrostatic Gating.

In this article, we report on a comprehensive modeling study of frequency tuning of graphene resonant nanoelectromechanical systems (NEMS) via electrostatic coupling forces induced by controlling the voltage of a capacitive gate. The model applies to both doubly clamped graphene membranes and circumference-clamped circular drumhead device structures. Frequency tuning of these devices can be predicted by considering both capacitive softening and elastic stiffening. It is shown that the built-in strain in the device strongly dictates the frequency tuning behavior and tuning range. We also find that doubly clamped graphene resonators can have a wider frequency tuning range, while circular drumhead devices have higher initial resonance frequency with same device characteristic parameters. Further, the parametric study in this work clearly shows that a smaller built-in strain, smaller depth of air gap or cavity, and larger device size or characteristic length (e.g., length for doubly clamped devices, and diameter for circular drumheads) help achieve a wider range of electrostatic frequency tunability. This study builds a solid foundation that can offer important device fabrication and design guidelines for achieving radio frequency components (e.g., voltage controlled oscillators and filters) with the desired frequencies and tuning ranges.