scispace - formally typeset
Y

Yu Huang

Researcher at University of Texas Health Science Center at Houston

Publications -  19
Citations -  1075

Yu Huang is an academic researcher from University of Texas Health Science Center at Houston. The author has contributed to research in topics: Dielectrophoresis & Context (archaeology). The author has an hindex of 11, co-authored 14 publications receiving 953 citations. Previous affiliations of Yu Huang include Chinese Academy of Sciences & University of Texas MD Anderson Cancer Center.

Papers
More filters
Journal ArticleDOI

Introducing dielectrophoresis as a new force field for field-flow fractionation.

TL;DR: The validity of the model is demonstrated with human leukemia (HL-60) cells subjected to a parallel electrode array, and application of the device to separating HL-60 cells from peripheral blood mononuclear cells is shown.
Journal ArticleDOI

Dielectrophoretic manipulation of cells with spiral electrodes

TL;DR: It was shown that the conventional and traveling-wave dielectrophoretic force components dominated cell levitation and radial motion, respectively, and the cell radial velocity was very sensitive to the field frequency when the in-phase component of the field-induced polarization was close to zero.
Journal ArticleDOI

Extracellular Spermine Exacerbates Ischemic Neuronal Injury through Sensitization of ASIC1a Channels to Extracellular Acidosis

TL;DR: It is shown that extracellular spermine contributes significantly to ischemic neuronal injury through enhancing ASIC1a activity, and suggests new neuroprotective strategies for stroke patients via inhibition of polyamine synthesis and subsequent s permine–ASIC interaction.
Journal ArticleDOI

Tissue acidosis induces neuronal necroptosis via ASIC1a channel independent of its ionic conduction

TL;DR: It is shown that extracellular protons function as a novel endogenous ligand that triggers neuronal necroptosis during ischemia via ASIC1a, but independent of its ion-conducting function.
Journal ArticleDOI

PI3-kinase/Akt Pathway-Regulated Membrane Insertion of Acid-Sensing Ion Channel 1a Underlies BDNF-Induced Pain Hypersensitivity

TL;DR: It is shown that deletion of ASIC1 gene suppressed the sustained mechanical hyperalgesia induced by intrathecal BDNF application in mice, revealing a novel mechanism underlying central sensitization and pain hypersensitivity, and reinforcing the critical role of ASIC 1a channels in these processes.