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We report a synthesis method for the selective 6-endo cyclization of o-phenylacrylamides to obtain 3,4-dihydroquinolinones via aryl anions formed by two-electron reduction under electrochemistry using phenanthrene as the reduction mediator.

This paper presents a metasurface-based linear-to-circular polarization converter with a flexible structure for conformal and wearable applications. The converter consists of nested S- and C-shaped split ring resonators in the unit cell and can convert linearly polarized incident waves into left-handed circularly polarized ones at 12.4 GHz. Simulation results show that the proposed design has a high polarization conversion rate and efficiency at the operating frequency. Conformal tests are also conducted to evaluate the performance under curvature circumstances. A minor shift in the operating frequency is observed when the converter is applied on a sinusoidal wavy surface.

Modern smart grids are built based on top of advanced computing and networking technologies, where condition monitoring relies on secure cyberphysical connectivity. Over the network infrastructure, transported data containing confidential information, must be protected as smart grids are vulnerable and subject to various cyberattacks. Various machine learning based classifiers were proposed for intrusion detection in smart grids. However, each of them has respective advantage and disadvantages. Aiming to improve the performance of existing machine learning based classifiers, this paper proposes an adaptive deep learning algorithm with a data pre-processing module, a neural network pre-training module and a classifier module, which work together classify intrusion data types using their high-dimensional data features. The proposed Adaptive Deep Learning (ADL) algorithm obtains the number of layers and the number of neurons per layer by determining the characteristic dimension of the network traffic. With transfer learning, the proposed ADL algorithm can extract the original data dimensions and obtain new abstract features. By combining deep learning models with traditional machine learning-based classification models, the performance of classification of network traffic data is significantly improved. By using the Network Security Laboratory-Knowledge Discovery in Databases (NSL-KDD) dataset, experimental results show that the proposed ADL algorithm improves the effectiveness of existing intrusion detection methods and reduces the training time, indicating a promising candidate to enhance network security in smart grids.

BackgroundBiallelic mutations in CYP27A1 and CYP7B1, two critical genes regulating cholesterol and bile acid metabolism, cause cerebrotendinous xanthomatosis (CTX) and hereditary spastic paraplegia type 5 (SPG5), respectively. These rare diseases are characterized by progressive degeneration of corticospinal motor neuron axons, yet the underlying pathogenic mechanisms and strategies to mitigate axonal degeneration remain elusive.MethodsTo generate induced pluripotent stem cell (iPSC)-based models for CTX and SPG5, we reprogrammed patient skin fibroblasts into iPSCs by transducing fibroblast cells with episomal vectors containing pluripotency factors. These patient-specific iPSCs, as well as control iPSCs, were differentiated into cortical projection neurons (PNs) and examined for biochemical alterations and disease-related phenotypes.ResultsCTX and SPG5 patient iPSC-derived cortical PNs recapitulated several disease-specific biochemical changes and axonal defects of both diseases. Notably, the bile acid chenodeoxycholic acid (CDCA) effectively mitigated the biochemical alterations and rescued axonal degeneration in patient iPSC-derived neurons. To further examine underlying disease mechanisms, we developed CYP7B1 knockout human embryonic stem cell (hESC) lines using CRISPR-cas9-mediated gene editing and, following differentiation, examined hESC-derived cortical PNs. Knockout of CYP7B1 resulted in similar axonal vesiculation and degeneration in human cortical PN axons, confirming a cause-effect relationship between gene deficiency and axonal degeneration. Interestingly, CYP7B1 deficiency led to impaired neurofilament expression and organization as well as axonal degeneration, which could be rescued with CDCA, establishing a new disease mechanism and therapeutic target to mitigate axonal degeneration.ConclusionsOur data demonstrate disease-specific lipid disturbances and axonopathy mechanisms in human pluripotent stem cell-based neuronal models of CTX and SPG5 and identify CDCA, an established treatment of CTX, as a potential pharmacotherapy for SPG5. We propose this novel treatment strategy to rescue axonal degeneration in SPG5, a currently incurable condition. Background: Biallelic mutations in CYP27A1 and CYP7B1, two critical genes regulating cholesterol and bile acid metabolism, cause cerebrotendinous xanthomatosis (CTX) and hereditary spastic paraplegia type 5 (SPG5), respectively. These rare diseases are characterized by progressive degeneration of corticospinal motor neuron axons, yet the underlying pathogenic mechanisms and strategies to mitigate axonal degeneration remain elusive. Methods: To generate induced pluripotent stem cell (iPSC)-based models for CTX and SPG5, we reprogrammed patient skin fibroblasts into iPSCs by transducing fibroblast cells with episomal vectors containing pluripotency factors. These patient-specific iPSCs, as well as control iPSCs, were differentiated into cortical projection neurons (PNs) and examined for biochemical alterations and disease-related phenotypes. Results: CTX and SPG5 patient iPSC-derived cortical PNs recapitulated several disease-specific biochemical changes and axonal defects of both diseases. Notably, the bile acid chenodeoxycholic acid (CDCA) effectively mitigated the biochemical alterations and rescued axonal degeneration in patient iPSC-derived neurons. To further examine underlying disease mechanisms, we developed CYP7B1 knockout human embryonic stem cell (hESC) lines using CRISPR-cas9-mediated gene editing and, following differentiation, examined hESC-derived cortical PNs. Knockout of CYP7B1 resulted in similar axonal vesiculation and degeneration in human cortical PN axons, confirming a cause-effect relationship between gene deficiency and axonal degeneration. Interestingly, CYP7B1 deficiency led to impaired neurofilament expression and organization as well as axonal degeneration, which could be rescued with CDCA, establishing a new disease mechanism and therapeutic target to mitigate axonal degeneration. Conclusions: Our data demonstrate disease-specific lipid disturbances and axonopathy mechanisms in human pluripotent stem cell-based neuronal models of CTX and SPG5 and identify CDCA, an established treatment of CTX, as a potential pharmacotherapy for SPG5. We propose this novel treatment strategy to rescue axonal degeneration in SPG5, a currently incurable condition.

Hereditary spastic paraplegias are characterized by lower limb spasticity resulting from degeneration of long corticospinal axons. SPG11 is one of the most common autosomal recessive hereditary spastic paraplegias, and the SPG11 protein spatacsin forms a complex with the SPG15 protein spastizin and heterotetrameric AP5 adaptor protein complex, which includes the SPG48 protein AP5Z1. Using the integration-free episomal method, we established SPG11 patient-specific induced pluripotent stem cells (iPSCs) from patient fibroblasts. We differentiated SPG11 iPSCs, as well as SPG48 iPSCs previously established, into cortical projection neurons and examined protective effects by targeting mitochondrial dynamics using P110, a peptide that selectively inhibits mitochondrial fission GTPase Drp1. P110 treatment mitigates mitochondrial fragmentation, improves mitochondrial motility, and restores mitochondrial health and ATP levels in SPG11 and SPG48 neurons. Neurofilament aggregations are increased in SPG11 and SPG48 axons, and these are also suppressed by P110. Similarly, P110 mitigates neurofilament disruption in both SPG11 and SPG48 knockdown cortical projection neurons, confirming the contribution of hereditary spastic paraplegia gene deficiency to subsequent neurofilament and mitochondrial defects. Strikingly, neurofilament aggregations in SPG11 and SPG48 deficient neurons double stain with ubiquitin and autophagy related proteins, resembling the pathological hallmark observed in SPG11 autopsy brain sections. To confirm the cause-effect relationship between the SPG11 mutations and disease phenotypes, we knocked-in SPG11 disease mutations to human embryonic stem cells (hESCs) and differentiated these stem cells into cortical projection neurons. Reduced ATP levels and accumulated neurofilament aggregations along axons are observed, and both are mitigated by P110. Furthermore, rescue experiment with expression of wild-type SPG11 in cortical projection neurons derived from both SPG11 patient iPSCs and SPG11 disease mutation knock-in hESCs leads to rescue of mitochondrial dysfunction and neurofilament aggregations in these SPG11 neurons. Finally, in SPG11 and SPG48 long-term cultures, increased release of phosphoNF-H, a biomarker for nerve degeneration, is significantly reduced by inhibiting mitochondrial fission pharmacologically using P110 and genetically using Drp1 shRNA. Taken together, our results demonstrate that impaired mitochondrial dynamics underlie both cytoskeletal disorganization and axonal degeneration in SPG11 and SPG48 neurons, highlighting the importance of targeting these pathologies therapeutically.

Patients with diabetes are confronted with numerous obstacles to achieve adequate glycemic control during hospitalization. The aim of this study was to explore the risk factors associated with glycemic control in hospitalized patients with type 2 diabetes mellitus (T2DM) treated with continuous subcutaneous insulin infusion (CSII).This cross-sectional study included 5223 patients hospitalized with T2DM in a tertiary hospital in Xiamen (China) between January 2017 and December 2019. All patients were managed according to established protocols for glycemic monitoring and insulin pump treatment regimens. Demographic information and clinical profiles were collected from electronic health records. Multiple linear regression analysis was used to identify the risk factors associated with glycemic control.Among the 5223 hospitalized patients with T2DM receiving CSII therapy, 55.2% achieved their ideal blood glucose level (3.9-10.0 mmol/L), 44.5% experienced hyperglycemia ( 10.0 mmol/L), and 0.3% experienced hypoglycemia ( 3.9 mmol/L) during their hospitalization. Multivariate analyses showed that among inpatients with T2DM, older age, male gender, higher low-density lipoprotein-cholesterol (LDL-C) level, lower C-peptide (C-P) level, lower body mass index (BMI), longer duration of diabetes, previous insulin prescriptions, nephropathy, and retinopathy were factors more likely to be associated with a blood glucose level in the hyperglycemic range (P 0.05). We also observed that among hospitalized patients with T2DM, those with lower BMI, lower C-P, lower LDL-C, longer disease duration, and previous insulin prescriptions were more likely to correlate with a higher proportion of hypoglycemia range (all P 0.05).Older age, male gender, lower BMI, lower C-P, higher LDL-C, previous insulin prescriptions, longer duration of diabetes, nephropathy, and retinopathy may be risk factors for a higher proportion of hyperglycemic events in hospitalized patients with T2DM under CSII therapy. Furthermore, lower BMI, lower C-P, lower LDL-C, longer duration of diabetes, and previous insulin prescriptions were found to be important factors for a higher proportion of hypoglycemic events. Evaluating the clinical features, comorbidities, and complications of hospitalized patients is essential to achieve reasonable glycemic control.

This randomized clinical trial assesses the long-term effect of vigorous and moderate exercise on incident diabetes over a 10-year follow-up after a 12-month exercise intervention.

The last decade has witnessed an increasing number of wireless standards for civil, military, and space communications. Along with the advances in integrated circuit (IC) technologies and the ever-growing requirements of high data rates, next-generation radios are expected to operate over multiple frequency bands. For example, carrier aggregation is used in LTE-Advanced radios to increase the bandwidth. However, it is challenging for traditional radios to operate over multiple frequency bands. In response to this, software-defined radios (SDRs) have been proposed to handle multiple bands through reconfiguration. They can adapt carrier frequency, transmission bandwidth, modulation, and encoding schemes by modifying digital signal processing (DSP) software algorithms [1]. In contrast to SDR, legacy communication systems are approaching their capability limits. They usually operate on a single band and require dedicated hardware. Thus, SDR is a promising radio technology to increase the flexibility of radio devices and reduce hardware and manufacturing costs, chip size, and power consumption [2].

This article presents a scalable ultra-high-frequency (UHF) radio frequency identification (RFID) reader antenna for retail checkout counters. The antenna’s simultaneous near-field and far-field operation enable effortless and reliable asset identification. Two meandered microstrip lines that are 90° out-of-phase form the near-field antenna rim around a far-field patch antenna. The patch antenna is fed by those meandered lines along the vertices on its orthogonal points, resulting in circular polarization. The near-field radiation is evenly distributed with no surface dead zones, and the far-field radiation pattern is symmetrical with a 90° half-power beam-width in both azimuth and elevation planes. The antenna operates in the North American UHF RFID band (902-928 MHz) with a 50 MHz impedance bandwidth. Fabricated antenna’s gain and axial ratio at the band’s center frequency of 915 MHz is 3.3 dBi, and 1.4 dB, respectively. This antenna is low-profile, low-cost and recyclable as it is constructed from polyolefin substrate and copper foils. The antenna is pragmatic, scalable with increasing checkout counter sizes and insusceptible to proximity assets and metal frames.

At present, the ultrahigh frequency (UHF) radio-frequency identification (RFID) technology is more popular than several other autoidentification (auto-ID) technologies. An ultrarugged UHF RFID reader antenna is made from a concrete substrate that is sandwiched between a stubbed quarterwave radiator and a folded ground plane is proposed for fixed UHF RFID readers. This linearly polarized antenna operates between 865 and 868 MHz with a 3.5-dBi peak gain and a 160-MHz, -15-dB |S11| bandwidth. The 3.5- and 2-dBi gain bandwidth are 80 and 140 MHz, respectively. The antenna is intended to be used in convention center loading docks and is thus tested for extreme environmental conditions, such as temperature, humidity, condensation, and rain as well as the effect of superstrates and metals. More than one concrete tile antenna can be operated by using one RFID reader to realize a distributed antenna system (DAS). The antenna is conformal and can blend with the environment without affecting the existing aesthetics. The antenna creates a wide circumferential read zone (s5.6-m diameter) and reads tags up to 6.5 m at the boresight in free space.

This paper presents a compact frequency reconfigurable antenna for flexible devices and conformal surfaces. The antenna consists of a simple easy to fabricate structure consisting of a stub loaded circular radiator, designed on commercially available RT5880 flexible substrate ( $\varepsilon _{\mathrm {r}} = 2.2$ ) with a thickness of 0.254 mm. The combination of stub loading and slot etching techniques are utilized to achieve the advantages of compactness, frequency reconfigurability, wide impedance bandwidth, and stable radiation pattern with structural conformability. The frequency reconfigurability is achieved by employing two p-i-n diodes. Simulated and experimental results showed that the antenna operates in various important commercial bands, such as S-band (2 GHz– 4 GHz), Wi-Max (3.5 GHz and 5.8 GHz), Wi-Fi (3.6 GHz, 5 GHz, and 5.9 GHz), 5G sub-6-GHz (3.5 GHz and 4.4 GHz – 5 GHz), and ITU-band (7.725 GHz – 8.5 GHz) with the additional advantages of structural conformability. Furthermore, the performance comparison of the proposed flexible antenna with the state-of-the-art flexible antennas in terms of compactness, frequency reconfigurability, and number of operating bands demonstrates the novelty of the proposed antenna and its potential application in heterogeneous applications.

Hereditary spastic paraplegias (HSPs), a heterogeneous group of neurological disorders, are caused by axonal degeneration involving the long corticospinal tract which leads to the progressive spasticity and weakness of lower limbs. Over 80 different gene loci associated with HSP have been identified. Studying various HSP proteins reveals several common cellular themes in these debilitating diseases including vesicular trafficking, organelle shaping and morphogenesis, lipid/cholesterol metabolism, and endolysosomal and autophagic dysfunction. Though animal and cell models have been developed to study HSP, it remains a challenge to obtain patient-specific cortical neurons that are specifically affected and impaired in HSP. Recently, the discovery of induced pluripotent stem cells (iPSCs) provides a promising tool in neurological disease modeling due to their ability of self-renewal and capability of differentiation into various cell types. HSP patient iPSC-derived cortical projection neurons offer a unique source for HSP modeling to understand the molecular and cellular mechanisms, reveal neuronal pathological phenotypes, and test potential drugs. Here, we will introduce HSP and different common cellular themes, summarize in vitro HSP models using human pluripotent stem cells, and discuss the current challenges and future directions of HSP iPSC modeling.

Axonal degeneration underlies many debilitating diseases including hereditary spastic paraplegias (HSPs). HSPs are a large heterogeneous group of neurodegenerative diseases characterized by axonopathy involving the long corticospinal tract. How axons of these cortical projection neurons specifically degenerate in HSPs remains largely unclear partially due to the lack of human models to monitor the dynamic process of axonal degeneration. With the development of induced pluripotent stem cell (iPSC) technology, patient-specific iPSCs are successfully generated from HSP patients, providing a unique paradigm to study the axonal degeneration in patient-derived neurons in live cultures. In this chapter, we will summarize the procedures to examine axonal defects in iPSC models of HSPs and discuss the challenges and future applications in order to rescue axonal degeneration in HSPs.

The flourish of mobile communications is driven by the increasing number of subscribers and rapid advance of electronic devices. This brings up many multimedia context-aware services, among which real time locating system (RTLS) has become necessary in many applications. To locate a mobile station (MS), RTLS could apply conventional fingerprinting algorithm using received signal strength indicator (RSSI), which allows a MS to collect RSSI data from beacons sent by access points (APs). However, this method does not work for iPhones because of the lack of open access to Apple application programming interface (API) to obtain RSSI values. This paper proposes an alternative approach, under which APs in the monitoring mode are used to collect RSSI values for semi-beacon packets sent from a MS. We implement the packet capture library, which enables us to obtain RSSI values of semi-beacon packets sent by an iPhone. With a region-based k-nearest neighbor (kNN) localization algorithm, we successfully locate an iPhone user in indoor environment. In addition, experimental results show that the proposed approach outperforms the conventional RSSI fingerprinting approach.

Charcot-Marie-Tooth (CMT) disease is one of the most common genetically inherited neurological disorders and CMT type 2A (CMT 2A) is caused by dominant mutations in the mitofusin-2 (MFN2) gene. MFN2 is located in the outer mitochondrial membrane and is a mediator of mitochondrial fusion, with an essential role in maintaining normal neuronal functions. Although loss of MFN2 induces axonal neuropathy, the detailed mechanism by which MFN2 deficiency results in axonal degeneration of human spinal motor neurons remains largely unknown. In this study, we generated MFN2-knockdown human embryonic stem cell (hESC) lines using lentivirus expressing MFN2 short hairpin RNA (shRNA). Using these hESC lines, we found that MFN2 loss did not affect spinal motor neuron differentiation from hESCs but resulted in mitochondrial fragmentation and dysfunction as determined by live-cell imaging. Notably, MFN2-knockodwn spinal motor neurons exhibited CMT2A disease-related phenotypes, including extensive perikaryal inclusions of phosphorylated neurofilament heavy chain (pNfH), frequent axonal swellings, and increased pNfH levels in long-term cultures. Importantly, MFN2 deficit impaired anterograde and retrograde mitochondrial transport within axons, and reduced the mRNA and protein levels of kinesin and dynein, indicating the interfered motor protein expression induced by MFN2 deficiency. Our results reveal that MFN2 knockdown induced axonal degeneration of spinal motor neurons and defects in mitochondrial morphology and function. The impaired mitochondrial transport in MFN2-knockdown spinal motor neurons is mediated, at least partially, by the altered motor proteins, providing potential therapeutic targets for rescuing axonal degeneration of spinal motor neurons in CMT2A disease.

A compact frequency reconfigurable printed antenna for millimeter-wave applications is presented in this paper. This design is obtained by the merging of a half-arc and a right-angled triangle patch extracted from a rectangular radiator. The design approach is based on the use of two S-PIN diodes to obtain frequency reconfigurability. The antenna exhibits seven reconfigurable bands while showing good performances in terms of return loss, bandwidth and gain. The proposed antenna is well suited for future fifth-generation (5G) networks because of its notable features of small overall size (7.5 \(\times\) 5 \(\times\) 0.762 mm3), wide bandwidth, and frequency reconfigurability.

This paper presents the design and realization of a compact frequency reconfigurable antenna for multiband wireless applications. The antenna can operate at overall eight different bands in four dual-band modes. A slot in the radiator and defected ground structure are utilized to achieve a compact size, while PIN diodes are used for frequency reconfigurability in the proposed antenna. The antenna shows broad bandwidth in each operating frequency and has a compact size of 18 mm × 18 mm × 1.524 mm. Moreover, stable radiation patterns and a high value of efficiency make it a potential candidate for various wireless applications. Furthermore, to demonstrate the worth of this work, its performance is compared with state-of-the-art designs reported for similar applications.

Motor neurons are large projection neurons classified into upper and lower motor neurons responsible for controlling the movement of muscles. Degeneration of motor neurons results in progressive muscle weakness, which underlies several debilitating neurological disorders including amyotrophic lateral sclerosis (ALS), hereditary spastic paraplegias (HSP), and spinal muscular atrophy (SMA). With the development of induced pluripotent stem cell (iPSC) technology, human iPSCs can be derived from patients and further differentiated into motor neurons. Motor neuron disease models can also be generated by genetically modifying human pluripotent stem cells. The efficiency of gene targeting in human cells had been very low, but is greatly improved with recent gene editing technologies such as zinc-finger nucleases (ZFN), transcription activator-like effector nucleases (TALEN), and CRISPR-Cas9. The combination of human stem cell-based models and gene editing tools provides unique paradigms to dissect pathogenic mechanisms and to explore therapeutics for these devastating diseases. Owing to the critical role of several genes in the etiology of motor neuron diseases, targeted gene therapies have been developed, including antisense oligonucleotides, viral-based gene delivery, and in situ gene editing. This review summarizes recent advancements in these areas and discusses future challenges toward the development of transformative medicines for motor neuron diseases.

This Letter presents the design and analysis of a tunable low noise amplifier (LNA) capable of achieving single band, dual band and wideband operations. The circuit features a modified tunable open stub matching to achieve a reconfigurable multiband response. The LNA adopts a varactor diode in the input matching stage to achieve reconfigurable modes. Two bias conditions for the varactor diode are analysed. The forward bias condition yields a wideband mode (1.6 to 2.5 GHz) and zero bias results in a concurrent dual band mode (0.9 and 1.7–2.5 GHz). In reverse bias condition, the bias voltage of varactor diode ( V d − rb ) can be tuned to achieve one single band mode (1 GHz), and a tunable concurrent dual band mode, where the first band is fixed at 1 GHz and the second band is continuously tunable from 1.7 to 2.5 GHz. The LNA is fabricated in microwave integrated circuit process on an FR-4 board. The measured power gain is 7–15 dB and noise figure is 1.2–2.2 dB across all bands. The measured 1 dB compression ( P 1 dB ) is − 4 , − 3 and − 6 dBm at 0.9, 1 and 2.4 GHz, respectively.

High-performance antennas operating at ultra-high frequency (UHF) are typically designed and fabricated using specialized radio frequency (RF) materials with low loss and consistent properties. This paper proposes and investigates the use of recycled polyolefin (high-density polyethylene and polypropylene) which is not specifically manufactured for RF applications and thus with unknown RF properties, as dielectric substrate for high-performance UHF patch antennas. As a demonstrative application, a polarization-reconfigurable patch antenna with dual feeds is designed and fabricated using adhesive copper foil on recycled polyolefin substrate. Depending on the feed's magnitude and phase, different types of linear and circular polarizations can be achieved. The point of resonance for both ports is centered at 915 MHz with 10 dB return loss and bandwidth of 28 MHz. Port isolation is as low as −17 dB with peak linear and circular gain of 7.0 dBi, and 7 dBiC, respectively, observed in all polarizations. The resulting antenna not only performs well, but is also lightweight, low moisture absorbent, mechanically sturdy, inexpensive and ecologically friendly arising from its use of recycled materials.

Spinal muscular atrophy (SMA), the leading genetic cause of infant mortality, is characterized by the deterioration of alpha motor neurons in the brainstem and spinal cord. Currently, there is no cure for SMA, which calls for an urgent need to explore affordable and effective therapies and to maximize patients' independence and quality of life. Adeno-associated virus (AAV) vector, one of the most promising and well-investigated vehicles for delivering transgenes, is a compelling candidate for gene therapy. Some of the hallmarks of AAVs are their nonpathogenicity, inability to incur an immune response, potential to achieve robust transgene expression, and varied tropism for several tissues of the body. Recently, these features were harnessed in a clinical trial conducted by AveXis in SMA patients, where AAV9 was employed as a vehicle for one-time administration of the SMN gene, the causative gene in SMA. The trial demonstrated remarkable improvements in motor milestones and rates of survival in the patients. This review focuses on the advent of SMA gene therapy and summarizes different preclinical studies that were conducted leading up to the AAV9-SMA trial in SMA patients.

This research article proposes a compact frequency and pattern reconfigurable flexible antenna for heterogeneous applications. A triangular monopole antenna with a semicircular stub is made frequency and pattern tunable by connecting and disconnecting two inverted L-shaped stubs utilizing diodes. When either of the stubs is connected to the radiator, a relative phase difference happens at both ends of the radiator that changes the direction of the electromagnetic radiations, consequently pattern reconfigurability can be obtain. Besides that, because of the reactive load introduced by the stubs, the antenna’s effective length has changed and, as a result, the frequency reconfigurability can be attained. The antenna features a compact size of 40 × 50 × 0.254 mm3 corresponding to 0.22λo × 0.27λo × 0.001λo, where λo is free-space wavelength at 1.65 GHz, while its operational bandwidth is from 1.65 GHz to 2.51 GHz, with an average gain and radiation efficiency of better than 2.2 dBi and 80%, exhibiting a pattern reconfigurability of 180° in the E-plane. The frequency of the proposed antenna can be switched from 2.1 GHz to 1.8 GHz by switching the state of both diodes in OFF and ON-state, respectively. The fabricated prototype of the antenna is tested to verify its performance parameters. In addition, to validate the proposed design, it has been compared with prior arts in terms of the overall size, reconfigurability type, flexibility, radio frequency (RF) switch type used for reconfigurability, and frequency bandwidth. The proposed antenna provides smaller size with a large bandwidth coverage alongside with discrete RF switch type with the advantages of flexibility and both frequency and pattern reconfigurability. As a result, the proposed compact flexible and pattern reconfigurable antenna is a promising candidate for heterogeneous applications, including the global system for mobile (GSM) band (1800 and 1900 MHz) and industrial, scientific and medical (ISM) band (2.4 GHz) along with well-known cellular communication bands of 3G, 4G, and long term evolution (LTE) bands ranging from 1700–2300 MHz around the globe.

This article belongs to the Special Issue Millimeter-wave and Terahertz Applications of Metamaterials. This paper presents the design and realization of a compact size multimode frequency reconfigurable antenna. The antenna consists of a triangular-shaped monopole radiator, originally inspired from a rectangular monopole antenna. Slots were utilized to notch the desired frequency while the PIN diodes were utilized to achieve frequency reconfigurability. The antenna can operate in wideband, dual-band, or tri-band mode depending upon the state of the diodes. To validate the simulation results, a prototype was fabricated, and various performance parameters were measured and compared with simulated results. The strong agreement between simulated and measured results along with superior performance as compared to existing works in the literature makes the proposed antenna a strong candidate for ISM, 5G-sub-6 GHz, and S-band applications. This work is partially supported by RTI2018-095499-B-C31, Funded by Ministerio de Ciencia, Innovación y Universidades, Gobierno de España (MCIU/AEI/FEDER,UE).