We propose and empirically support a parsimonious account of intrinsic, brain-wide spatiotemporal organization arising from traveling waves linked to arousal. We hypothesize that these waves are the predominant physiological process reflected in spontaneous functional magnetic resonance imaging (fMRI) signal fluctuations. The correlation structure ("functional connectivity") of these fluctuations recapitulates the large-scale functional organization of the brain. However, a unifying physiological account of this structure has so far been lacking. Here, using fMRI in humans, we show that ongoing arousal fluctuations are associated with global waves of activity that slowly propagate in parallel throughout the neocortex, thalamus, striatum, and cerebellum. We show that these waves can parsimoniously account for many features of spontaneous fMRI signal fluctuations, including topographically organized functional connectivity. Last, we demonstrate similar, cortex-wide propagation of neural activity measured with electrocorticography in macaques. These findings suggest that traveling waves spatiotemporally pattern brain-wide excitability in relation to arousal.Transmembrane proteins play vital roles in mediating synaptic transmission, plasticity, and homeostasis in the brain. However, these proteins, especially the G protein-coupled receptors (GPCRs), are underrepresented in most large-scale proteomic surveys. Here, we present a new proteomic approach aided by deep learning models for comprehensive profiling of transmembrane protein families in multiple mouse brain regions. Our multiregional proteome profiling highlights the considerable discrepancy between messenger RNA and protein distribution, especially for region-enriched GPCRs, and predicts an endogenous GPCR interaction network in the brain. Furthermore, our new approach reveals the transmembrane proteome remodeling landscape in the brain of a mouse depression model, which led to the identification of two previously unknown GPCR regulators of depressive-like behaviors. Our study provides an enabling technology and rich data resource to expand the understanding of transmembrane proteome organization and dynamics in the brain and accelerate the discovery of potential therapeutic targets for depression treatment.Unsupported Pt electrocatalysts demonstrate excellent electrochemical stability when used in polymer electrolyte membrane fuel cells; however, their extreme thinness and low porosity result in insufficient surface area and high mass transfer resistance. Here, we introduce three-dimensionally (3D) customized, multiscale Pt nanoarchitectures (PtNAs) composed of dense and narrow (for sufficient active sites) and sparse (for improved mass transfer) nanoscale building blocks. The 3D-multiscale PtNA fabricated by ultrahigh-resolution nanotransfer printing exhibited excellent performance (45% enhanced maximum power density) and high durability (only 5% loss of surface area for 5000 cycles) compared to commercial Pt/C. We also theoretically elucidate the relationship between the 3D structures and cell performance using computational fluid dynamics. We expect that the structure-controlled 3D electrocatalysts will introduce a new pathway to design and fabricate high-performance electrocatalysts for fuel cells, as well as various electrochemical devices that require the precision engineering of reaction surfaces and mass transfer. This randomized trial compared ultrasound-guided pericapsular nerve group block and suprainguinal fascia iliaca block in patients undergoing primary total hip arthroplasty. We selected the postoperative incidence of quadriceps motor block (defined as paresis or paralysis of knee extension) at 6 hours as the primary outcome. We hypothesized that, compared with suprainguinal fascia iliaca block, pericapsular nerve group block would decrease its occurrence from 70% to 20%. Forty patients undergoing primary total hip arthroplasty under spinal anesthesia were randomly allocated to receive a pericapsular nerve group block (n=20) using 20 mL of adrenalized levobupivacaine 0.50%, or a suprainguinal fascia iliaca block (n=20) using 40 mL of adrenalized levobupivacaine 0.25%. After the performance of the block, a blinded observer recorded pain scores at 3, 6, 12, 18, 24, 36, and 48 hours; cumulative breakthrough morphine consumption at 24 and 48 hours; opioid-related side effects; ability to perform physiotherapy alts in better preservation of motor function than suprainguinal fascia iliaca block. Additional investigation is required to elucidate the optimal local anesthetic volume for motor-sparing pericapsular nerve group block and to compare the latter with alternate motor-sparing strategies such as periarticular local anesthetic infiltration. NCT04402450.NCT04402450.Cell-to-cell transmission of α-synuclein (α-syn) pathology is considered to underlie the spread of neurodegeneration in Parkinson's disease (PD). Previous studies have demonstrated that α-syn is secreted under physiological conditions in neuronal cell lines and primary neurons. However, the molecular mechanisms that regulate extracellular α-syn secretion remain unclear. In this study, we found that inhibition of monoamine oxidase-B (MAO-B) enzymatic activity facilitated α-syn secretion in human neuroblastoma SH-SY5Y cells. Both inhibition of MAO-B by selegiline or rasagiline and siRNA-mediated knock-down of MAO-B facilitated α-syn secretion. However, TVP-1022, the S-isomer of rasagiline that is 1000 times less active, failed to facilitate α-syn secretion. Additionally, the MAO-B inhibition-induced increase in α-syn secretion was unaffected by brefeldin A, which inhibits endoplasmic reticulum (ER)/Golgi transport, but was blocked by probenecid and glyburide, which inhibit ATP-binding cassette (ABC) transporterNT The identification of a neuroprotective agent that slows or stops the progression of motor impairments is required to treat Parkinson's disease (PD). The process of α-synuclein (α-syn) aggregation is thought to underlie neurodegeneration in PD. Here, we demonstrated that pharmacological inhibition or knock-down of monoamine oxidase-B (MAO-B) in SH-SY5Y cells facilitated α-syn secretion via a non-classical pathway involving an ATP-binding cassette (ABC) transporter. MAO-B inhibition preferentially facilitated secretion of detergent-insoluble α-syn protein and reduced its intracellular accumulation under chloroquine-induced lysosomal dysfunction. Additionally, MAO-B inhibition by selegiline protected A53T α-syn-induced nigrostriatal dopaminergic neuronal loss and suppressed the formation and cell-to-cell transmission of α-syn aggregates in rat models. check details We therefore propose a new function of MAO-B inhibition that modulates α-syn secretion and aggregation.