Fanningjonassen9647

Ju, Yang and Wang.The increasing prevalence of smart mobile devices (e.g., smartphones) enables the combined use of mobile crowdsensing (MCS) and ecological momentary assessments (EMA) in the healthcare domain. By correlating qualitative longitudinal and ecologically valid EMA assessment data sets with sensor measurements in mobile apps, new valuable insights about patients (e.g., humans who suffer from chronic diseases) can be gained. However, there are numerous conceptual, architectural and technical, as well as legal challenges when implementing a respective software solution. Therefore, the work at hand (1) identifies these challenges, (2) derives respective recommendations, and (3) proposes a reference architecture for a MCS-EMA-platform addressing the defined recommendations. The required insights to propose the reference architecture were gained in several large-scale mHealth crowdsensing studies running for many years and different healthcare questions. To mention only two examples, we are running crowdsensing studies on questions for the tinnitus chronic disorder or psychological stress. We consider the proposed reference architecture and the identified challenges and recommendations as a contribution in two respects. First, they enable other researchers to align our practical studies with a baseline setting that can satisfy the variously revealed insights. Second, they are a proper basis to better compare data that was gathered using MCS and EMA. In addition, the combined use of MCS and EMA increasingly requires suitable architectures and associated digital solutions for the healthcare domain. Copyright © 2020 Kraft, Schlee, Stach, Reichert, Langguth, Baumeister, Probst, Hannemann and Pryss.[This corrects the article DOI 10.3389/fnins.2019.01393.]. Copyright © 2020 Wang, Li, Guo, Zhang, Zhang, Zhu, Cheng, Yu, Ji and Tao.Current neural prostheses can restore limb movement to tetraplegic patients by translating brain signals coding movements to control a variety of actuators. Fast and accurate somatosensory feedback is essential for normal movement, particularly dexterous tasks, but is currently lacking in motor neural prostheses. Attempts to restore somatosensory feedback have largely focused on cortical stimulation which, thus far, have succeeded in eliciting minimal naturalistic sensations. Yet, a question that deserves more attention is whether the cortex is the best place to activate the central nervous system to restore somatosensation. Here, we propose that the brainstem dorsal column nuclei are an ideal alternative target to restore somatosensation. We review some of the recent literature investigating the dorsal column nuclei functional organization and neurophysiology and highlight some of the advantages and limitations of the dorsal column nuclei as a future neural prosthetic target. Recent evidence supports the dorsal column nuclei as a potential neural prosthetic target, but also identifies several gaps in our knowledge as well as potential limitations which need to be addressed before such a goal can become reality. Copyright © 2020 Loutit and Potas.Alzheimer's disease (AD), the most common form of dementia, is highly prevalent in older adults. The main clinical feature is the progressive decline of memory function, which eventually leads to the decline of cognitive function. At present, the pathogenesis of AD is unclear. In the disease process, synaptic changes are the key. Recent studies have shown that the dysregulation of RNA methylation is related to many biological processes, including neurodevelopment and neurodegenerative diseases. N6-methyladenosine (m6A) is the most abundant modification in eukaryotic RNA. In this study, RNA m6A methylation was quantified in APP/PS1 transgenic mice, which is an AD mouse model, and C57BL/6 control mice, and data showed that m6A methylation was elevated in the cortex and the hippocampus of APP/PS1 transgenic mice. Next, the alterations of m6A RNA methylation in AD and in C57BL/6 mice were investigated using high-throughput sequencing. Genome-wide maps of m6A mRNA showed that the degrees of m6A methylation were higher in many genes and lower in others in AD mice. BTK inhibitor libraries Interestingly, the expression of the m6A methyltransferase METTL3 was elevated and that of the m6A demethylase FTO was decreased in AD mice. The data were analyzed by gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses, and pathways that might be related to synaptic or neuron development and growth were constructed. The related pathways and genes predicted the potential roles of the differentially expressed m6A methylation RNA in AD. Collectively, our findings demonstrate that the m6A methylation of RNA promotes the development of AD. Copyright © 2020 Han, Liu, Xu, Liu, Wang, Li, Wang and Bi.Studies demonstrated that spinal autophagy was impaired in spinal nerve ligation (SNL) rats. However, the relationship of endoplasmic reticulum (ER) stress and ER-phagy and whether dexmedetomidine (DEX) modulates ER-phagy remain unclear. In this study, male Sprague-Dawley (SD) rats and the SNL animal model were used. 4-Phenylbutyric acid (4-PBA), tunicamycin (TM), rapamycin (RAP), and 3-methyladenine (3-MA) were intrathecally administered, respectively to demonstrate the relationship of ER stress and ER-phagy. Dexmedetomidine (30 μg/kg) was administered as treatment. Mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) tests were performed to evaluate nociceptive hypersensitivity. Protein expressions were examined by Western blot, and the location of glucose-regulated protein 78 (Grp78) was examined by immunofluorescence staining. SNL induced ER stress and ER-phagy impairment. ER stress was altered in rostral ventromedial medulla (RVM); 4-phenylbutyric acid induced analgesic effect via inhibiting ER stress and unfolded protein response (UPR) pathways to induce ER-phagy; tunicamycin led to worsening pain through enhancing ER stress and UPR pathways to further impair ER-phagy. Rapamycin provided analgesic effect through enhancing ER-phagy to relieve SNL-induced ER stress and UPR pathway activation; 3-methyladenine deteriorated pain via further impairing ER-phagy to aggravate ER stress. Dexmedetomidine provided analgesic effect through elevating ER-phagy. In conclusion, ER stress led to ER-phagy impairment in the spinal cord of SNL rats and participated in the nociceptive descending system. ER-phagy impairment was both a trigger and an effector of ER stress via UPR pathways in SNL rats. Dexmedetomidine targeted ER-phagy to provide analgesic effect. Copyright © 2020 Liu, Wang, Wang, Ding, Li, Guo, Han and Zhao.