A multimode metamaterial for a compact and robust dualband wireless power transfer system.

To release more flexibility for users to charge their portable devices, researchers have increasingly developed compact wireless power transfer (WPT) systems in recent years. Also, a dual-band WPT system is proposed to transfer power and signal simultaneously, enriching the system's functionality. Moreover, a stacked metasurface has recently been proposed for a single band near-field WPT system. In this study, a novel multimode self-resonance-enhanced wideband metasurface is proposed for a robust dual-band WPT system, which significantly improves the performance of both bands. The size of the transmitter (Tx) and the receiver (Rx) are both 15 mm × 15 mm only. The proposed metasurface can improve efficiency from 0.04 up to 39% in the best case. The measured figure of merit (FoM) is 2.09 at 390 MHz and 2.16 at 770 MHz, respectively, in the balanced mode. Especially, the FoM can reach up to 4.34 in the lower mode. Compared to the previous state-of-the-art for similar applications, the WPT performance has significantly been improved.

Analysis and design of diode physical limit bandwidth efficient rectification circuit for maximum flat efficiency, wide impedance, and efficiency bandwidths.

Generally, a conventional voltage doubler circuit possesses a large variation of its input impedance over the bandwidth, which results in limited bandwidth and low RF-dc conversion efficiency. A basic aspect for designing wideband voltage doubler rectifiers is the use of complex matching circuits to achieve decade and octave impedance and RF-dc conversion efficiency bandwidths. Still, the reported techniques till now have been accompanied by a large fluctuation of the RF-dc conversion efficiency over the operating bandwidth. In this paper, we propose a novel rectification circuit with minimal inter-stage matching that consists of a single short-circuit stub and a virtual battery, which contributes negligible losses and overcomes these existing problems. Consequently, the proposed rectifier circuit achieves a diode physical-limit-bandwidth efficient rectification. In other words, the rectification bandwidth, as well as the peak efficiency, are controlled by the length of the stub and the physical limitation of the diodes.

Wireless power transfer system rigid to tissue characteristics using metamaterial inspired geometry for biomedical implant applications.

Conventional resonant inductive coupling wireless power transfer (WPT) systems encounter performance degradation while energizing biomedical implants. This degradation results from the dielectric and conductive characteristics of the tissue, which cause increased radiation and conduction losses, respectively. Moreover, the proximity of a resonator to the high permittivity tissue causes a change in its operating frequency if misalignment occurs. In this report, we propose a metamaterial inspired geometry with near-zero permeability property to overcome these mentioned problems. This metamaterial inspired geometry is stacked split ring resonator metamaterial fed by a driving inductive loop and acts as a WPT transmitter for an in-tissue implanted WPT receiver. The presented demonstrations have confirmed that the proposed metamaterial inspired WPT system outperforms the conventional one. Also, the resonance frequency of the proposed metamaterial inspired TX is negligibly affected by the tissue characteristics, which is of great interest from the design and operation prospects. Furthermore, the proposed WPT system can be used with more than twice the input power of the conventional one while complying with the safety regulations of electromagnetic waves exposure.

Critical analysis of the use of ß-site amyloid precursor protein-cleaving enzyme 1 inhibitors in the treatment of Alzheimer's disease.

Alzheimer's disease (AD) is the major cause of dementia in the elderly and an unmet clinical challenge. A variety of therapies that are currently under development are directed to the amyloid cascade. Indeed, the accumulation and toxicity of amyloid-ß (Aß) is believed to play a central role in the etiology of the disease, and thus rational interventions are aimed at reducing the levels of Aß in the brain. Targeting ß-site amyloid precursor protein-cleaving enzyme (BACE)-1 represents an attractive strategy, as this enzyme catalyzes the initial and rate-limiting step in Aß production. Observation of increased levels of BACE1 and enzymatic activity in the brain, cerebrospinal fluid, and platelets of patients with AD and mild cognitive impairment supports the potential benefits of BACE1 inhibition. Numerous potent inhibitors have been generated, and many of these have been proved to lower Aß levels in the brain of animal models. Over 10 years of intensive research on BACE1 inhibitors has now culminated in advancing half a dozen of these drugs into human trials, yet translating the in vitro and cellular efficacy of BACE1 inhibitors into preclinical and clinical trials represents a challenge. This review addresses the promises and also the potential problems associated with BACE1 inhibitors for AD therapy, as the complex biological function of BACE1 in the brain is becoming unraveled.

Decreased expression of GGA3 protein in Alzheimer's disease frontal cortex and increased co-distribution of BACE with the amyloid precursor protein.

BACE initiates the amyloidogenic processing of the amyloid precursor protein (APP) that results in the production of Aß peptides associated with Alzheimer's disease (AD). Previous studies have indicated that BACE is elevated in the frontal cortex of AD patients. Golgi-localized γ-ear containing ADP ribosylation factor-binding proteins (GGA) control the cellular trafficking of BACE and may alter its levels. To investigate a link between BACE and GGA expression in AD, frontal cortex samples from AD (N = 20) and healthy, age-matched controls (HC, N =17) were analyzed by immunoblotting. After normalization to the neuronal marker ß-tubulin III, the data indicate an average two-fold increase of BACE protein (p = 0.01) and a 64% decrease of GGA3 in the AD group compared to the HC (p = 0.006). GGA1 levels were also decreased in AD, but a statistical significance was not achieved. qRT-PCR analysis of GGA3 mRNA showed no difference between AD and HC. There was a strong correlation between GGA1 and GGA3 in both AD and HC, but no correlation between BACE and GGA levels. Subcellular fractionation of AD cortex with low levels of GGA proteins showed an alteration of BACE distribution and extensive co-localization with APP. These data suggest that altered compartmentalization of BACE in AD promotes the amyloidogenic processing of APP.

Decreased Neuregulin 1 C-terminal fragment in Brodmann's area 6 of patients with schizophrenia.

Neuregulin 1 (NRG1) is a susceptibility gene for schizophrenia. A decrease in NRG1-ErbB4 signalling has also been associated with the disease. ß-amyloid precursor protein-cleaving enzyme (BACE1) processes type III NRG1 precursor, a major neuregulin variant expressed in the brain, to release NRG1 fragments that trigger signalling events and activation of neurotransmitter receptors. Experimental evidence suggests that muscarinic acetylcholine receptors (CHRM) regulate BACE1 expression. Having recently shown that CHRM1 levels are decreased selectively in frontal cortex regions of a subpopulation of schizophrenic patients (muscarinic receptor deficit schizophrenia, MRDS) we aimed to compare the protein expression of BACE1 and NRG1 in the agranular frontal cortex Brodmann's area 6 of SCZ subjects with normal levels of CHRM1 (N = 19), MRDS (N = 20), and age/gender-matched non-psychiatric (healthy) controls (HC; N = 20). Western blot analysis of post-mortem samples showed that the levels of BACE1 and full-length NRG1 precursor (130 kDa) did not differ significantly between the three groups. In contrast, the levels of the NRG1 C-terminal fragment (NRG1-CTF) were decreased by approximately 50% in both schizophrenic groups compared to the HC group (p<0.0027). The ratio of NRG1-CTF versus NRG1 precursor was significantly reduced in the SCZ groups compared to the HC group (p = 0.051). There was no correlation between the levels of either full-length NRG1, NRG1-CTF, or BACE1 and the final recorded doses of antipsychotic drugs for the subjects with schizophrenia. A positive correlation was found between BACE1 and full-length NRG1 precursor in the HC group (r(2) = 0.671, p<0.001) but not in the schizophrenic groups. These data suggest that the proteolytic processing of NRG1 is impaired in schizophrenia.

BACE: Therapeutic target and potential biomarker for Alzheimer's disease.

ß-Site APP-cleaving enzyme (BACE) is a membrane-bound aspartyl protease involved in the production of Alzheimer's disease (AD) Aß amyloid peptides. This enzyme is ubiquitously expressed, with highest levels in the brain and pancreas. Its cellular trafficking is tightly controlled as it recycles between endosomes and trans-Golgi network. BACE expression increases in response to aging and various stress stimuli. It is elevated in the brain cortex of AD sufferers, and increased levels of BACE in the cerebrospinal fluid of patients with mild cognitive impairment may provide an early biomarker of AD. BACE is considered as a rational drug target for AD therapy, and inhibitors are under development. Anomalies in the behaviour and biochemistry of BACE(-/-) mice have pointed to the role this enzyme plays in the processing of neuregulin and of voltage-gated sodium channel ß-subunit. A full understanding of BACE biology in health and disease is needed to establish a safe AD therapy based on BACE inhibitors.