Results 91 to 100 of about 144,323 (265)
An activity‐dependent pathway links prefrontal circuit hypoactivity to cognitive impairment. Reduced PVA–mPFC activity upregulates NEPAS, which suppresses PTX3 secretion, leading to impaired angiogenesis, myelin deficits, and memory decline. Rescue is achieved by NEPAS knockdown or chemogenetic circuit activation.
Boya Hu +11 more
wiley +1 more source
Abstract Dynamin 1 is a GTPase protein involved in synaptic vesicle fission, which facilitates the exocytosis of neurotransmitters necessary for normal signaling. Pathogenic variants in the DNM1 gene are associated with intractable epilepsy, often manifested as infantile spasms at onset, developmental delay, and a movement disorder, and are located in ...
Davide Mei +4 more
wiley +1 more source
Laser‐induced graphene (LIG) provides a scalable, laser‐direct‐written route to porous graphene architecture with tunable chemistry and defect density. Through heterojunction engineering, catalytic functionalization, and intrinsic self‐heating, LIG achieves highly sensitive and selective detection of NOX, NH3, H2, and humidity, supporting next ...
Md Abu Sayeed Biswas +6 more
wiley +1 more source
This study presents a miniaturized bidirectional thermal stimulation system integrated with an electrode array enabling real‐time, bidirectional modulation and simultaneous recording of neural activity through localized heating and cooling. By monolithic integration of the Peltier element and with a silicon neural probe, the innovative system allows ...
Zoia Naumkina +6 more
wiley +1 more source
Amuc_1473 Links Gut Microbes to Skeletal Homeostasis and Counteracts Multifactorial Osteoporosis
Amuc_1473, a previously uncharacterized protein enriched in Akkermansia muciniphila‐derived extracellular vesicles, is identified as a gut–bone messenger that promotes osteogenesis and inhibits osteoclastogenesis by engaging transcriptional and translational regulators in bone cells.
Shan‐Shan Rao +28 more
wiley +1 more source
mGluR5 in ECCCK to BLA Circuit Modulates Depressive‐Like Phenotypes through CCK Signaling
Dysregulation of mGluR5 and CCK signaling contributes to major depressive disorder, yet circuit‐level mechanisms remain unclear. Here, the ECCCK→BLA pathway is identified as a critical regulator of affective behavior. mGluR5 modulates synaptic function and CCK signaling within this circuit, controlling stress susceptibility and depressive‐like states ...
Muhammad Asim +4 more
wiley +1 more source
Bone cancer pain and depression share a common origin: astrocytic A2‐to‐A1 transition in the posterior piriform cortex. This phenotypic shift disrupts the ATP–adenosine–A2AR–norepinephrine axis, simultaneously driving nociceptive and affective dysfunction.
Jiang‐Ping Liu +14 more
wiley +1 more source
Slow‐transit constipation (STC) is a disabling motility disorder with unclear smooth‐muscle mechanisms. Spatial proteomic analysis of STC patient colon reveals both the central pathogenic role of smooth muscle cells (SMCs) in STC and novel regulators of intestinal motility, BIN1 and ALDH1B1.
Jianbo Liu +10 more
wiley +1 more source
Multimodal Imaging Reveals Rapid Catecholamine Uptake and Release by Neutrophils
We show that immune cells (neutrophils) synthesize, uptake, and store catecholamine neurotransmitters such as dopamine or adrenaline. They also release them in response to specific stimuli (serotonin), which we directly visualize using fluorescent nanosensors. We further demonstrate that catecholamines affect neutrophil functions (NETosis) and platelet
Jennifer Mohr +19 more
wiley +1 more source
Smart Nanotechnologies for Multimodal Neuromodulation and Brain Interfacing
Recent advances in smart nanotechnologies are expanding the toolbox for brain interfacing, from wireless neuromodulation and high‐resolution sensing to targeted delivery within the central nervous system. By combining responsive nanomaterials with bioinspired design, these platforms enable multimodal interactions with neurons and glia, while also ...
Tommaso Curiale +6 more
wiley +1 more source

