We developed a real-time sleep stage classification system with a convolutional neural network using only a one-channel electro-encephalogram source from mice and universally available features in any time-series data raw signal, spectrum, and zeitgeber time. To accommodate historical information from each subject, we included a long short-term memory recurrent neural network in combination with the universal features. The resulting system (UTSN-L) achieved 90% overall accuracy and 81% multi-class Matthews Correlation Coefficient, with particularly high-quality judgements for rapid eye movement sleep (91% sensitivity and 98% specificity). This system can enable automatic real-time interventions during rapid eye movement sleep, which has been difficult due to its relatively low abundance and short duration. Further, it eliminates the need for ordinal pre-calibration, electromyogram recording, and manual classification and thus is scalable. The code is open-source with a graphical user interface and closed feedback loop capability, making it easily adaptable to a wide variety of end-user needs. By allowing large-scale, automatic, and real-time sleep stage-specific interventions, this system can aid further investigations of the functions of sleep and the development of new therapeutic strategies for sleep-related disorders.N-glycosylation of glycoproteins, a major post-translational modification, plays a crucial role in various biological phenomena. SW-100 in vivo In central nervous systems, N-glycosylation is thought to be associated with differentiation and regeneration; however, the state and role of N-glycosylation in neuronal differentiation remain unclear. Here, we conducted sequential LC/MS/MS analyses of tryptic digest, enriched glycopeptides, and deglycosylated peptides of proteins derived from human-induced pluripotent stem cells (iPSCs) and iPSC-derived neuronal cells, which were used as a model of neuronal differentiation. We demonstrate that the production profiles of many glycoproteins and their glycoforms were altered during neuronal differentiation. Particularly, the levels of glycoproteins modified with an N-glycan, consisting of five N-acetylhexosamines, three hexoses, and a fucose (HN5H3F), increased in dopaminergic neuron-rich cells (DAs). The N-glycan was deduced to be a fucosylated and bisected biantennary glycan based on product ion spectra. Interestingly, the HN5H3F-modified proteins were predicted to be functionally involved in neural cell adhesion, axon guidance, and the semaphorin-plexin signaling pathway, and protein modifications were site-selective and DA-selective regardless of protein production levels. Our integrated method for glycoproteome analysis and resultant profiles of glycoproteins and their glycoforms provide valuable information for further understanding the role of N-glycosylation in neuronal differentiation and neural regeneration.We recently identified a kidney risk inflammatory signature (KRIS), comprising 6 TNF receptors (including TNFR1 and TNFR2) and 11 inflammatory proteins. Elevated levels of these proteins in circulation were strongly associated with risk of the development of end-stage kidney disease (ESKD) during 10-year follow-up. It has been hypothesized that elevated levels of these proteins in circulation might reflect (be markers of) systemic exposure to TNFα. In this in vitro study, we examined intracellular and extracellular levels of these proteins in human umbilical vein endothelial cells (HUVECs) exposed to TNFα in the presence of hyperglycemia. KRIS proteins as well as 1300 other proteins were measured using the SOMAscan proteomics platform. Four KRIS proteins (including TNFR1) were down-regulated and only 1 protein (IL18R1) was up-regulated in the extracellular fraction of TNFα-stimulated HUVECs. In the intracellular fraction, one KRIS protein was down-regulated (CCL14) and 1 protein was up-regulated (IL18R1). The levels of other KRIS proteins were not affected by exposure to TNFα. HUVECs exposed to a hyperglycemic and inflammatory environment also showed significant up-regulation of a distinct set of 53 proteins (mainly in extracellular fraction). In our previous study, circulating levels of these proteins were not associated with progression to ESKD in diabetes.In individuals with a musculoskeletal disorder, goal-directed reaching movements of the hand are distorted. Here, we investigated a pain-related fear-conditioning effect on motor control. Twenty healthy participants (11 women and 9 men, 21.7 ± 2.7 years) performed a hand-reaching movement task. In the acquisition phase, a painful electrocutaneous stimulus was applied on the reaching hand simultaneous with the completion of reaching. In the subsequent extinction phase, the task context was the same but the painful stimulus was omitted. We divided the kinematic data of the hand-reaching movements into acceleration and deceleration periods based on the movement-velocity characteristics, and the duration of each period indicated the degree of impairment in the feedforward and feedback motor controls. We assessed the wavelet coherence between electromyograms of the triceps and biceps brachii muscles. In the acquisition phase, the durations of painful movements were significantly longer in both the acceleration and deceleration periods. In the extinction phase, painful movements were longer only in the acceleration period and higher pain expectation and fear were maintained. Similarly, the wavelet coherence of muscles in both periods were decreased in both the acquisition and extinction phases. These results indicate that negative emotional modulations might explain the altered motor functions observed in pain patients.A growing body of evidence indicates that cellular metabolism is involved in immune cell functions, including cytokine production. Serine is a nutritionally non-essential amino acid that can be generated by de novo synthesis and conversion from glycine. Serine contributes to various cellular responses, but the role in inflammatory responses remains poorly understood. Here, we show that macrophages rely on extracellular serine to suppress aberrant cytokine production. Depleting serine from the culture media reduced the cellular serine content in macrophages markedly, suggesting that macrophages depend largely on extracellular serine rather than cellular synthesis. Under serine deprivation, macrophages stimulated with lipopolysaccharide showed aberrant cytokine expression patterns, including a marked reduction of anti-inflammatory interleukin-10 expression and sustained expression of interleukine-6. Transcriptomic and metabolomics analyses revealed that serine deprivation causes mitochondrial dysfunction reduction in the pyruvate content, the NADH/NAD+ ratio, the oxygen consumption rate, and the mitochondrial production of reactive oxygen species (ROS).