Yu Huang

Bio: Yu Huang is an academic researcher from Chinese Academy of Sciences. The author has contributed to research in topics: Medicine & Materials science. The author has an hindex of 136, co-authored 1492 publications receiving 89209 citations. Previous affiliations of Yu Huang include The Chinese University of Hong Kong & Samsung.

Antioxidant activity of flavonoids isolated from Scutellaria rehderiana

Abstract: The present study examined the antioxidant activity in heated canola oil of hexane, acetone, and methanol extracts of dry roots of gansu huangqin (Scutellaria rehderiana) as well as six flavonoids isolated from the acetone and methanol extracts. The oxidation was conducted at 95°C by monitoring oxygen consumption and decreases in both linoleic and α-linolenic acids. The acetone extract was most effective in inhibiting oxidation of canola oil, followed by the methanol extract. The antioxidant activity of gansu huangqin acetone extract was dose-dependent. Among the six flavonoids, baicalein and ganhuangenin were more effective than butylated hydroxytoluene (BHT) in protecting canola oil from oxidation. The present results suggest that the acetone extract of this root may be a potential source of natural antioxidants for use in processed foods.

Peptide-Assisted 2-D Assembly toward Free-Floating Ultrathin Platinum Nanoplates as Effective Electrocatalysts.

Abstract: We demonstrate the 2-D anisotropic formation of ultrathin free-floating Pt nanoplates from the assembly of small nanocrystals using T7 peptide (Ac-TLTTLTN-CONH2). As-formed nanoplates are rich in grain boundaries that can promote their catalytic activities. Furthermore, we demonstrate that a minor number of Pd atoms can selectively deposit on and stabilize the grain boundaries, which leads to enhanced structure stability. The Pd-enhanced Pt polycrystal nanoplates show great oxygen reduction reaction activities with 15.5 times higher specific activity and 13.7 times higher mass activity than current state-of-the-art commercial Pt/C electrocatalysts as well as 2.5 times higher mass activity for hydrogen evolution reaction compared with Pt/C.

Depletion of intracellular Ca2+ stores enhances flow-induced vascular dilatation in rat small mesenteric artery.

Abstract: The effect of depleting intracellular Ca2+ stores on flow-induced vascular dilatation and the mechanism responsible for the vasodilatation were examined in rat isolated small mesenteric arteries. The arteries were pressurized to 50 mmHg and preconstricted with phenylephrine. Intraluminal flow reversed the effect of phenylephrine, resulting in vasodilatation. Flow dilatation consisted of an initial transient peak followed by a sustained plateau phase. The magnitude of dilatation was markedly reduced by removing Ca2+ from the intraluminal flow medium. Depletion of intracellular Ca2+ stores with either cyclopiazonic acid (CPA, 2 μM) or 1,4-dihydroxy-2,5-di-tert-butylbenzene (BHQ, 10 μM) significantly augmented the magnitude of flow dilatation. Flow-induced endothelial cell Ca2+ influx was also markedly enhanced in arteries pretreated with CPA or BHQ. Flow-induced dilatation was insensitive to Nw-nitro-L-arginine methyl ester (100 μM) plus indomethacin (3 μM) or to oxyhemoglobin (3 μM), but was markedly reduced by 30 mM extracellular K+ or 2 mM tetrabutylammonium (TBA), suggesting an involvement of EDHF. Catalase at 1200 U ml−1 abolished the flow-induced dilatation, while the application of exogenous H2O2 (90–220 μM) induced relaxation in phenylephrine-preconstricted arteries. Relaxation to exogenous H2O2 was blocked in the presence of 30 mM extracellular K+, and H2O2 (90 μM) hyperpolarized the smooth muscle cells, indicating that H2O2 can act as an EDHF. In conclusion, flow-induced dilatation in rat mesenteric arteries can be markedly enhanced by prior depletion of intracellular Ca2+ stores. Furthermore, these data are consistent with a role for H2O2 as the vasodilator involved. British Journal of Pharmacology (2006) 147, 506–515. doi:10.1038/sj.bjp.0706639

Genetic lineage tracing discloses arteriogenesis as the main mechanism for collateral growth in the mouse heart

Abstract: Aims Capillary and arterial endothelial cells share many common molecular markers in both the neonatal and adult hearts. Herein, we aim to establish a genetic tool that distinguishes these two types of vessels in order to determine the cellular mechanism underlying collateral artery formation. Methods and results Using Apln-GFP and Apln-LacZ reporter mice, we demonstrate that APLN expression is enriched in coronary vascular endothelial cells. However, APLN expression is reduced in coronary arterial endothelial cells. Genetic lineage tracing, using an Apln-CreER mouse line, robustly labelled capillary endothelial cells, but not arterial endothelial cells. We leveraged this differential activity of Apln-CreER to study collateral artery formation following myocardial infarction (MI). In a neonatal heart MI model, we found that Apln-CreER-labelled capillary endothelial cells do not contribute to the large collateral arteries. Instead, these large collateral arteries mainly arise from pre-existing, infrequently labelled coronary arteries, indicative of arteriogenesis. Furthermore, in an adult heart MI model, Apln-CreER activity also distinguishes large and small diameter arteries from capillaries. Lineage tracing in this setting demonstrated that most large and small coronary arteries in the infarcted myocardium and border region are derived not from capillaries, but from pre-existing arteries. Conclusion Apln-CreER-mediated lineage tracing distinguishes capillaries from large arteries, in both the neonatal and adult hearts. Through genetic fate mapping, we demonstrate that pre-existing arteries, but not capillaries, extensively contribute to collateral artery formation following myocardial injury. These results suggest that arteriogenesis is the major mechanism underlying collateral vessel formation.

I and i

Abstract: There is, I think, something ethereal about i —the square root of minus one. I remember first hearing about it at school. It seemed an odd beast at that time—an intruder hovering on the edge of reality. Usually familiarity dulls this sense of the bizarre, but in the case of i it was the reverse: over the years the sense of its surreal nature intensified. It seemed that it was impossible to write mathematics that described the real world in …

Fast parallel algorithms for short-range molecular dynamics

Abstract: Three parallel algorithms for classical molecular dynamics are presented. The first assigns each processor a fixed subset of atoms; the second assigns each a fixed subset of inter-atomic forces to compute; the third assigns each a fixed spatial region. The algorithms are suitable for molecular dynamics models which can be difficult to parallelize efficiently—those with short-range forces where the neighbors of each atom change rapidly. They can be implemented on any distributed-memory parallel machine which allows for message-passing of data between independently executing processors. The algorithms are tested on a standard Lennard-Jones benchmark problem for system sizes ranging from 500 to 100,000,000 atoms on several parallel supercomputers--the nCUBE 2, Intel iPSC/860 and Paragon, and Cray T3D. Comparing the results to the fastest reported vectorized Cray Y-MP and C90 algorithm shows that the current generation of parallel machines is competitive with conventional vector supercomputers even for small problems. For large problems, the spatial algorithm achieves parallel efficiencies of 90% and a 1840-node Intel Paragon performs up to 165 faster than a single Cray C9O processor. Trade-offs between the three algorithms and guidelines for adapting them to more complex molecular dynamics simulations are also discussed.

疟原虫var基因转换速率变化导致抗原变异[英]／Paul H, Robert P, Christodoulou Z, et al//Proc Natl Acad Sci U S A

Abstract: 抗原变异可使得多种致病微生物易于逃避宿主免疫应答。表达在感染红细胞表面的恶性疟原虫红细胞表面蛋白1（PfPMP1）与感染红细胞、内皮细胞、树突状细胞以及胎盘的单个或多个受体作用，在黏附及免疫逃避中起关键的作用。每个单倍体基因组var基因家族编码约60种成员，通过启动转录不同的var基因变异体为抗原变异提供了分子基础。