Method for time-of-flight estimation of low frequency acoustic signals in reverberant and noisy environment with sparse impulse response

For acoustic procedures which rely on the speed of sound to derive process parameters, the determination of the acoustic time of flight is essential. In this work, a method for the determination of the time of flight (TOF) is presented. It is intended for reverberant and noisy environments and can be applied in the gas holdup determination in bubbly liquids via acoustic transmission tomography (GHATT) for example. The method includes the selection and design of the transmitted signal to optimize the disambiguate of the autocorrelation, the narrowing of the time window based on the Fractional Fourier Transform (FrFT) to accelerate the TOF estimation. Furthermore, it includes the consideration of the system-induced signal distortion through prior quasi-anechoic measurements and the sparse reconstruction of the spatial impulse response for TOF estimation using non-negative sparse deconvolution algorithms. The method is tested analytically on numerically generated signals and various sparse deconvolution algorithms are investigated with respect to their applicability and limitations.

Prions and Neurodegenerative Diseases: A Focus on Alzheimer’s Disease

Specific protein misfolding and aggregation are mechanisms underlying various neurodegenerative diseases such as prion disease and Alzheimer’s disease (AD). The misfolded proteins are involved in prions, amyloid-β (Aβ), tau, and α-synuclein disorders; they share common structural, biological, and biochemical characteristics, as well as similar mechanisms of aggregation and self-propagation. Pathological features of AD include the appearance of plaques consisting of deposition of protein Aβ and neurofibrillary tangles formed by the hyperphosphorylated tau protein. Although it is not clear how protein aggregation leads to AD, we are learning that the cellular prion protein (PrPC) plays an important role in the pathogenesis of AD. Herein, we first examined the pathogenesis of prion and AD with a focus on the contribution of PrPC to the development of AD. We analyzed the mechanisms that lead to the formation of a high affinity bond between Aβ oligomers (AβOs) and PrPC. Also, we studied the role of PrPC as an AβO receptor that initiates an AβO-induced signal cascade involving mGluR5, Fyn, Pyk2, and eEF2K linking Aβ and tau pathologies, resulting in the death of neurons in the central nervous system. Finally, we have described how the PrPC-AβOs interaction can be used as a new potential therapeutic target for the treatment of PrPC-dependent AD.

Characterization of Vegard strain related to exceptionally fast Cu-chemical diffusion in Cu$$_2$$Mo$$_6$$S$$_8$$ by an advanced electrochemical strain microscopy method

Electrochemical strain microscopy (ESM) has been developed with the aim of measuring Vegard strains in mixed ionic-electronic conductors (MIECs), such as electrode materials for Li-ion batteries, caused by local changes in the chemical composition. In this technique, a voltage-biased AFM tip is used in contact resonance mode. However, extracting quantitative strain information from ESM experiments is highly challenging due to the complexity of the signal generation process. In particular, electrostatic interactions between tip and sample contribute significantly to the measured ESM signals, and the separation of Vegard strain-induced signal contributions from electrostatically induced signal contributions is by no means a trivial task. Recently, we have published a compensation method for eliminating frequency-independent electrostatic contributions in ESM measurements. Here, we demonstrate the potential of this method for detecting Vegard strain in MIECs by choosing Cu$$_2$$ 2 Mo$$_6$$ 6 S$$_8$$ 8 as a model-type MIEC with an exceptionally high Cu chemical diffusion coefficient. Even for this material, Vegard strains are only measurable around and above room-temperature and with proper elimination of electrostatics. The analyis of the measured Vegards strains gives strong indication that due to a high charge transfer resistance at the tip/interface, the local Cu concentration variations are much smaller than predicted by the local Nernst equation. This suggests that charge transfer resistances have to be analyzed in more detail in future ESM studies.

Pushing the Limits of Long Range Wireless Sensing with LoRa

Wireless sensing is an exciting new research area which enables a large variety of applications ranging from coarse-grained daily activity recognition to fine-grained vital sign monitoring. While promising in many aspects, one critical issue is the limited sensing range because weak reflection signals are used for sensing. Recently, LoRa signals are exploited for wireless sensing, moving a big step towards long-range sensing. Although promising, there is still a huge room for improvement. In this work, we qualitatively characterize the relationship between target movements and target-induced signal variations, and propose signal processing methods to enlarge the induced signal variation to achieve a longer sensing range. Experiment results show that the proposed system (1) pushes the contact-free sensing range of human walking from the state-of-the-art 50 m to 120 m; (2) achieves a sensing range of 75 m for fine-grained respiration sensing; and (3) demonstrates human respiration sensing even through seven concrete walls.

Lowering the thermal noise barrier in functional brain mapping with magnetic resonance imaging

Functional magnetic resonance imaging (fMRI) has become an indispensable tool for investigating the human brain. However, the inherently poor signal-to-noise-ratio (SNR) of the fMRI measurement represents a major barrier to expanding its spatiotemporal scale as well as its utility and ultimate impact. Here we introduce a denoising technique that selectively suppresses the thermal noise contribution to the fMRI experiment. Using 7-Tesla, high-resolution human brain data, we demonstrate improvements in key metrics of functional mapping (temporal-SNR, the detection and reproducibility of stimulus-induced signal changes, and accuracy of functional maps) while leaving the amplitude of the stimulus-induced signal changes, spatial precision, and functional point-spread-function unaltered. We demonstrate that the method enables the acquisition of ultrahigh resolution (0.5 mm isotropic) functional maps but is also equally beneficial for a large variety of fMRI applications, including supra-millimeter resolution 3- and 7-Tesla data obtained over different cortical regions with different stimulation/task paradigms and acquisition strategies.

Human Body–Electrode Interfaces for Wide-Frequency Sensing and Communication: A Review

Several on-body sensing and communication applications use electrodes in contact with the human body. Body–electrode interfaces in these cases act as a transducer, converting ionic current in the body to electronic current in the sensing and communication circuits and vice versa. An ideal body–electrode interface should have the characteristics of an electrical short, i.e., the transfer of ionic currents and electronic currents across the interface should happen without any hindrance. However, practical body–electrode interfaces often have definite impedances and potentials that hinder the free flow of currents, affecting the application’s performance. Minimizing the impact of body–electrode interfaces on the application’s performance requires one to understand the physics of such interfaces, how it distorts the signals passing through it, and how the interface-induced signal degradations affect the applications. Our work deals with reviewing these elements in the context of biopotential sensing and human body communication.

Trefoil Factor Family Member 2: From a High-Fat-Induced Gene to a Potential Obesity Therapy Target

Obesity has its epidemiological patterns continuously increasing. With controlling both diet and exercise being the main approaches to manage the energy metabolism balance, a high-fat (HF) diet is of particular importance. Indeed, lipids have a low satiety potential but a high caloric density. Thus, focusing on pharmacologically targetable pathways remains an approach with promising therapeutic potential. Within this context, trefoil factor family member 2 (Tff2) has been characterized as specifically induced by HF diet rather than low-fat diet. TFF2 has also been linked to diverse neurological mechanisms and metabolic patterns suggesting its role in energy balance. The hypothesis is that TFF2 would be a HF diet-induced signal that regulates metabolism with a focus on lipids. Within this review, we put the spotlight on key findings highlighting this line of thought. Importantly, the hypothetical mechanisms pointed highlight TFF2 as an important contributor to obesity development via increasing lipids intestinal absorption and anabolism. Therefore, an outlook for future experimental activities and evaluation of the therapeutic potential of TFF2 inhibition is given. Indeed, its knockdown or downregulation would contribute to an antiobesity phenotype. We believe this work represents an addition to our understanding of the lipidic molecular implications in obesity, which will contribute to develop therapies aiming to manage the lipidic metabolic pathways including the absorption, storage and metabolism via targeting TFF2-related pathways. We briefly discuss important relevant concepts for both basic and clinical researchers.

TRPV1 and TRPA1 Channels Are Both Involved Downstream of Histamine-Induced Itch

Two histamine receptor subtypes (HR), namely H1R and H4R, are involved in the transmission of histamine-induced itch as key components. Although exact downstream signaling mechanisms are still elusive, transient receptor potential (TRP) ion channels play important roles in the sensation of histaminergic and non-histaminergic itch. The aim of this study was to investigate the involvement of TRPV1 and TRPA1 channels in the transmission of histaminergic itch. The potential of TRPV1 and TRPA1 inhibitors to modulate H1R- and H4R-induced signal transmission was tested in a scratching assay in mice in vivo as well as via Ca2+ imaging of murine sensory dorsal root ganglia (DRG) neurons in vitro. TRPV1 inhibition led to a reduction of H1R- and H4R- induced itch, whereas TRPA1 inhibition reduced H4R- but not H1R-induced itch. TRPV1 and TRPA1 inhibition resulted in a reduced Ca2+ influx into sensory neurons in vitro. In conclusion, these results indicate that both channels, TRPV1 and TRPA1, are involved in the transmission of histamine-induced pruritus.