Browsing by Author "Chen, Shanshan"

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Dielectric Engineering of a Boron Nitride/Hafnium Oxide Heterostructure for High-Performance 2D Field Effect Transistors
(2016-03-09)
Zou, Xuming
;
Huang, Chun-Wei
;
Wang, Lifeng
;
Yin, Long-Jing
;
Li, Wenqing
A unique design of a hexagonal boron nitride (h-BN)/HfO2 dielectric heterostructure stack is demonstrated, with few-layer h-BN to alleviate the surface optical phonon scattering, followed by high-kappa HfO2 deposition to suppress Coulombic impurity scattering so that high-performance top-gated two-dimensional semiconductor transistors are achieved. Furthermore, this dielectric stack can also be extended to GaN-based transistors to enhance their performance.
High Mobility MoS2 Transistor with Low Schottky Barrier Contact by Using Atomic Thick h-BN as a Tunneling Layer
(2016-10-05)
Wang, Jingli
;
Yao, Qian
;
Huang, Chun-Wei
;
Zou, Xuming
;
Liao, Lei
High-performance MoS2 transistors are developed using atomic hexagonal boron nitride as a tunneling layer to reduce the Schottky barrier and achieve low contact resistance between metal and MoS2. Benefiting from the ultrathin tunneling layer within 0.6 nm, the Schottky barrier is significantly reduced from 158 to 31 meV with small tunneling resistance.
MicroRNA-483 amelioration of experimental pulmonary hypertension
(2020-05-08)
Zhang, Jin
;
He, Yangyang
;
Yan, Xiaosong
;
Chen, Shanshan
;
He, Ming
Endothelial dysfunction is critically involved in the pathogenesis of pulmonary arterial hypertension (PAH) and that exogenously administered microRNA may be of therapeutic benefit. Lower levels of miR-483 were found in serum from patients with idiopathic pulmonary arterial hypertension (IPAH), particularly those with more severe disease. RNA-seq and bioinformatics analyses showed that miR-483 targets several PAH-related genes, including transforming growth factor-beta (TGF-beta), TGF-beta receptor 2 (TGFBR2), beta-catenin, connective tissue growth factor (CTGF), interleukin-1 beta (IL-1 beta), and endothelin-1 (ET-1). Overexpression of miR-483 in ECs inhibited inflammatory and fibrogenic responses, revealed by the decreased expression of TGF-beta, TGFBR2, beta-catenin, CTGF, IL-1 beta, and ET-1. In contrast, inhibition of miR-483 increased these genes in ECs. Rats with EC-specific miR-483 overexpression exhibited ameliorated pulmonary hypertension (PH) and reduced right ventricular hypertrophy on challenge with monocrotaline (MCT) or Sugen + hypoxia. A reversal effect was observed in rats that received MCT with inhaled lentivirus overexpressing miR-483. These results indicate that PAH is associated with a reduced level of miR-483 and that miR-483 might reduce experimental PH by inhibition of multiple adverse responses.