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The Si‐based self‐powered broadband photodiode (SSBP) is prized for its ability to swiftly detect light across a wide spectrum without requiring an external voltage. However, boosting its efficiency remains challenging due to its high refractive index and limited UV light penetration. A combination of Si with ZnGa2O4, an ultra‐wide‐bandgap spinel material, can bring new opportunities to address these shortcomings of SSBP. In this study, a ZnGa2O4/p‐Si heterojunction photodiode is presented, which is capable of detecting UV to near‐infrared light autonomously. Operating without bias, this device exhibits excellent rectification and detects wavelengths from 265 to 1000 nm, achieving impressive performance metrics such as a photo‐to‐dark current ratio of 5.8 × 104, response speed of less than 3 ms, responsivity of 117 mA W−1, and specific detectivity of 5.5 × 1012 Jones while the photodiode demonstrates exceptional stability and durability under harsh conditions. The versatility of this device is demonstrated by applying it to the optical imaging sensors and physically unclonable security devices. This study provides new inspirations for the development of the energy‐efficient and emerging optical sensing technologies. [ABSTRACT FROM AUTHOR]

Electrocardiographic (ECG) R-peak detection is essential for every sensor-based cardiovascular health monitoring system. To validate R-peak detectors, comparing the predicted results with reference annotations is crucial. This comparison is typically performed using tools provided by the waveform database (WFDB) or custom methods. However, many studies fail to provide detailed information on the validation process. The literature also highlights inconsistencies in reporting window size, a crucial parameter used to compare predictions with expert annotations to distinguish false peaks from the true R-peak. Additionally, there is also a need for uniformity in reporting the total number of beats for individual or collective records of the widely used MIT-BIH arrhythmia database. Thus, we aim to review validation methods of various R-peak detection methodologies before their implementation in real time. This review discusses the impact of non-beat annotations when using a custom validation method, allowable window tolerance, the effects of window size deviations, and implications of varying numbers of beats and skipping segments on ECG testing, providing a comprehensive guide for researchers. Addressing these validation gaps is critical as they can significantly affect validatory outcomes. Finally, the conclusion section proposes a structured concept as a future approach, a guide to integrate WFDB R-peak validation tools for testing any QRS annotated ECG database. Overall, this review underscores the importance of complete transparency in reporting testing procedures, which prevents misleading assessments of R-peak detection algorithms and enables fair methodological comparison. [ABSTRACT FROM AUTHOR]

For the safe autonomous operations of unmanned aerial vehicles (UAVs) and ground control stations (GCS), including autonomous battery replacement, wireless power transfer, and more, the precise landing of UAVs on GCS is essential. Accurate landing is only possible when the link capacity strength exceeds a certain threshold, but this is often disturbed due to complex terrain. To address this, we developed an extremum seeking (ES)-based radio signal strength optimization (RSSO) algorithm, ES-RSSO, designed to find the optimal positions of the UAV using radio communication signals. This ensures energy-efficient path planning while guaranteeing the minimum received signal strength indication (RSSI) capacity. This algorithm is particularly useful in obstacle-rich environments, where UAVs are limited in power resources. Simulation results demonstrate a 2.37% decrease in the mean, a 62.08% improvement in variance, and a 3.72% decrease in the integration strength of the link capacity when ES-RSSO is applied. These results confirm that the RADIO.rssi maintenance ability remains above a critical boundary level, supporting robust communication links and energy-efficient path planning. Throughout the study, we showed how, in many cases, simply moving the UAV a few meters can significantly improve the communication link. [ABSTRACT FROM AUTHOR]

Animals sense chemical cues such as nutritious and noxious stimuli through the chemosensory system and adapt their behavior, physiology, and developmental schedule to the environment. In the Drosophila central nervous system, chemosensory interneurons that produce neuropeptides called Hugin (Hug) peptides receive signals from gustatory receptor neurons and regulate feeding behavior. Because Hug neurons project their axons to the higher brain region within the protocerebrum where dendrites of multiple neurons producing developmentally important neuropeptides are extended, it has been postulated that Hug neurons regulate development through the neuroendocrine system. In this study, we show that Hug neurons interact with a subset of protocerebrum neurons that produce prothoracicotropic hormone (PTTH) and regulate the onset of metamorphosis and systemic growth. Loss of the hug gene and silencing of Hug neurons caused a delay in larval‐to‐prepupal transition and an increase in final body size. Furthermore, deletion of Hug receptor‐encoding genes also caused developmental delay and body size increase, and the phenotype was restored by expressing Hug receptors in PTTH‐producing neurons. These results indicate that Hug neurons regulate developmental timing and body size via PTTH‐producing neurons. This study provides a basis for understanding how chemosensation is converted into neuroendocrine signaling to control insect growth and development. [ABSTRACT FROM AUTHOR]

The modern healthcare system strives to provide patients with more comfortable and less invasive experiences, focusing on noninvasive and painless diagnostic and treatment methods. A key priority is the early diagnosis of life-threatening diseases, which can significantly improve patient outcomes by enabling treatment at earlier stages. While most patients must undergo diagnostic procedures before beginning treatment, many existing methods are invasive, time-consuming, and inconvenient. To address these challenges, electrochemical-based wearable and point-of-care (PoC) sensing devices have emerged, playing a crucial role in the noninvasive, continuous, periodic, and remote monitoring of key biomarkers. Due to their numerous advantages, several wearable and PoC devices have been developed. In this focused review, we explore the advancements in metal–organic frameworks (MOFs)-based wearable and PoC devices. MOFs are porous crystalline materials that are cost-effective, biocompatible, and can be synthesized sustainably on a large scale, making them promising candidates for sensor development. However, research on MOF-based wearable and PoC sensors remains limited, and no comprehensive review has yet to synthesize the existing knowledge in this area. This review aims to fill that gap by emphasizing the design of materials, fabrication methodologies, sensing mechanisms, device construction, and real-world applicability of these sensors. Additionally, we underscore the importance and potential of MOF-based wearable and PoC sensors for advancing healthcare technologies. In conclusion, this review sheds light on the current state of the art, the challenges faced, and the opportunities ahead in MOF-based wearable and PoC sensing technologies. [ABSTRACT FROM AUTHOR]

Fluid clearance from the respiratory system during developmental transitions is critically important for achieving optimal gas exchange in animals. During insect development from embryo to adult, airway clearance occurs episodically each time the molt is completed by performance of the ecdysis sequence, coordinated by a peptide-signaling cascade initiated by ecdysis-triggering hormone (ETH). We find that the neuropeptide Kinin (also known as Drosokinin or Leukokinin) is required for normal respiratory fluid clearance or "tracheal air-filling" in Drosophila larvae. Disruption of Kinin signaling leads to defective air-filling during all larval stages. Such defects are observed upon ablation or electrical silencing of Kinin neurons, as well as RNA silencing of the Kinin gene or the ETH receptor in Kinin neurons, indicating that ETH targets Kinin neurons to promote tracheal air-filling. A Kinin receptor mutant fly line (Lkrf02594 ) also exhibits tracheal air-filling defects in all larval stages. Targeted Kinin receptor silencing in tracheal epithelial cells using breathless or pickpocket (ppk) drivers compromises tracheal air-filling. On the other hand, promotion of Kinin signaling in vivo through peptide injection or Kinin neuron activation through Drosophila TrpA1 (dTrpA1) expression induces premature tracheal collapse and air-filling. Moreover, direct exposure of tracheal epithelial cells in vitro to Kinin leads to calcium mobilization in tracheal epithelial cells. Our findings strongly implicate the neuropeptide Kinin as an important regulator of airway clearance via intracellular calcium mobilization in tracheal epithelial cells of Drosophila.

Chronic inflammation is deeply involved in various human disorders, such as cancer, neurodegenerative disorders, and metabolic disorders. Induction of epigenetic alterations, especially aberrant DNA methylation, is one of the major mechanisms, but how it is induced is still unclear. Here, we found that expression of TET genes, methylation erasers, was downregulated in inflamed mouse and human tissues, and that this was caused by upregulation of TET-targeting miRNAs such as MIR20A, MIR26B, and MIR29C, likely due to activation of NF-[kappa]B signaling downstream of IL-1[beta] and TNF-[alpha]. However, TET knockdown induced only mild aberrant methylation. Nitric oxide (NO), produced by NOS2, enhanced enzymatic activity of DNA methyltransferases (DNMTs), methylation writers, and NO exposure induced minimal aberrant methylation. In contrast, a combination of TET knockdown and NO exposure synergistically induced aberrant methylation, involving genomic regions not methylated by either alone. The results showed that a vicious combination of TET repression, due to NF-[kappa]B activation, and DNMT activation, due to NO production, is responsible for aberrant methylation induction in human tissues., Introduction Chronic inflammation is deeply involved in various human chronic disorders, such as cancer (1-3), neurodegenerative disorders (4), diabetes mellitus (5), and osteoarthritis (6). Induction of epigenetic alterations is considered [...]