Publications by authors named "Langzhou Liu"

Article Synopsis
  • - Ultrasound can deeply penetrate tissues to non-invasively influence cellular activities, making it a valuable tool in biomedical research.
  • - Combining ultrasound with nanomaterials allows for precise control over these activities using various stimuli like electric, optical, and chemical signals at a localized level.
  • - The article reviews the latest advancements in ultrasound technology paired with nanomaterials and discusses its potential applications in biology and medicine for research, diagnostics, and therapeutic purposes.
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Ultrasound is an acoustic wave which can noninvasively penetrate the skull to deep brain regions, enabling neuromodulation. However, conventional ultrasound's spatial resolution is diffraction-limited and low-precision. Here, we report acoustic nanobubble-mediated ultrasound stimulation capable of localizing ultrasound's effects to only the desired brain region in male mice.

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Numerous cellular processes are regulated by Ca signals, and the endoplasmic reticulum (ER) membrane's inositol triphosphate receptor (IPR) is critical for modulating intracellular Ca dynamics. The IPRs are seen to be clustered in a variety of cell types. The combination of IPRs clustering and IPRs-mediated Ca-induced Ca release results in the hierarchical organization of the Ca signals, which challenges the numerical simulation given the multiple spatial and temporal scales that must be covered.

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Astrocytic fine processes are the most minor structures of astrocytes but host much of the Ca activity. These localized Ca signals spatially restricted to microdomains are crucial for information processing and synaptic transmission. However, the mechanistic link between astrocytic nanoscale processes and microdomain Ca activity remains hazily understood because of the technical difficulties in accessing this structurally unresolved region.

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The accumulation of amyloid β peptide (Aβ) in the brain is hypothesized to be the major factor driving Alzheimer's disease (AD) pathogenesis. Mounting evidence suggests that astrocytes are the primary target of Aβ neurotoxicity. Aβ is known to interfere with multiple calcium fluxes, thus disrupting the calcium homeostasis regulation of astrocytes, which are likely to produce calcium oscillations.

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