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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.


Papers
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TL;DR: Enhancing the endothelial expression and function of SIRT1 prevents early vascular ageing and maintains vasodilator responses, thus representing promising drug targets for cardiovascular diseases.
Abstract: Aims Aged arteries are characterized by attenuated vasodilator and enhanced vasoconstrictor responses, which contribute to the development of diseases such as arterial hypertension, atherosclerosis, and heart failure SIRT1 is a longevity regulator exerting protective functions against vascular ageing, although the underlying mechanisms remain largely unknown This study was designed to elucidate the signalling pathways involved in endothelial SIRT1-mediated vasodilator responses in the arteries of young and old mice In particular, the contributions of nitric oxide (NO), endothelial NO synthase (eNOS), cyclooxygenase (COX), and/or soluble guanylyl cyclase (sGC) were examined Methods and results Wild type (WT) or eNOS knockout (eKO) mice were cross-bred with those overexpressing human SIRT1 selectively in the vascular endothelium (EC-SIRT1) Arteries were collected from the four groups of mice (WT, EC-SIRT1, eKO, and eKO-SIRT1) to measure isometric relaxations/contractions in response to various pharmacological agents Reduction of NO bioavailability, hyper-activation of COX signalling, and down-regulation of sGC collectively contributed to the decreased vasodilator and increased vasoconstrictor responses in arteries of old WT mice Overexpression of endothelial SIRT1 did not block the reduction in NO bioavailability but attenuated the hyper-activation of COX-2, thus protecting mice from age-induced vasoconstrictor responses in arteries of EC-SIRT1 mice Deficiency of eNOS did not affect endothelial SIRT1-mediated anti-contractile activities in arteries of eKO-SIRT1 mice Mechanistic studies revealed that overexpression of endothelial SIRT1 enhanced Notch signalling to up-regulate sGCβ1 in smooth muscle cells Increased expression and activity of sGC prevented age-induced hyper-activation of COX-2 as well as the conversion of endothelium-dependent relaxations to contractions in arteries of EC-SIRT1 mice Conclusion Age-induced down-regulation of sGC and up-regulation of COX-2 in arteries are at least partly attributable to the loss-of-endothelial SIRT1 function Enhancing the endothelial expression and function of SIRT1 prevents early vascular ageing and maintains vasodilator responses, thus representing promising drug targets for cardiovascular diseases

28 citations

Journal ArticleDOI
TL;DR: In this article, the authors explain the polar nature of chemical bonding and an implementation in classical and reactive atomistic simulations to understand such properties more quantitatively, using pairwise charge increments.
Abstract: Alloys are widely used in catalysts and structural materials. The nature of chemical bonding and the origin of alloy formation energies, defect energies, and interfacial properties have not been well understood to date but are critical to material performance. In this contribution, we explain the polar nature of chemical bonding and an implementation in classical and reactive atomistic simulations to understand such properties more quantitatively. Electronegativity differences between metal atoms lead to polar bonding, and exothermic alloy formation energies are related to charge transfer between the different elements. These differences can be quantified by atomic charges using pairwise charge increments, determined by matching the computed alloy formation energy to experimentally measured alloy formation energies using pair potentials for the pure metals. The polar character of alloys is comparable to organic molecules and partially ionic minerals, for example, AlNi and AlNi3 alloys assume significant a...

28 citations

Journal ArticleDOI
TL;DR: Interestingly, a thromboxane-prostanoid (TP) receptor blocker S18886 reversed SOPs-impaired vasorelaxation, suggesting the involvement of TP receptor in mediating the downstream effect.
Abstract: Aims β-Sitosterol has become a popular cholesterol-lowering functional food product worldwide. β-Sitosterol can be oxidized to β-sitosterol oxidation products (SOPs) during food processing. Little is known about the impact of SOPs and β-sitosterol on the functionality of arteries. This study investigated the effects of SOPs and β-sitosterol on vasorelaxation and the possible cellular mechanisms involved. Methods and results By isometric tension measurement, SOPs but not β-sitosterol blunted relaxation induced by acetylcholine or Ca2+ ionophore A23187 in endothelium-intact aortae. SOPs-impaired vasorelaxation was completely reversed by cyclooxygenase (COX)-2 inhibitor DuP-697, whereas the reversal by COX-1 inhibitor SC-560 was only partial. Western blotting and immunohistochemistry showed that SOPs increased the protein expression of COX-2 but not COX-1 in the endothelium. Using dihydroethidium staining and electron paramagnetic resonance spin trapping techniques, SOPs were found to elevate the level of reactive oxygen species in rat aortic endothelial cells, and the effects were reversed by antioxidants tempol, tiron, or diphenylene iodonium. Consistently, these antioxidants reversed SOPs-induced impairment of endothelium-dependent relaxation. Up-regulation of COX-2 expression by SOPs was also reversed by tempol. Moreover, SOPs attenuated nitric oxide donor sodium nitroprusside-induced relaxation in endothelium-intact, but not endothelium-denuded rings, confirming that SOPs act on the endothelium. Interestingly, a thromboxane-prostanoid (TP) receptor blocker S18886 reversed SOPs-impaired vasorelaxation, suggesting the involvement of TP receptor in mediating the downstream effect. SOPs decreased cGMP production, and the effect could be reversed by inhibiting COX-2 or TP receptor. Conclusion This study provides novel experimental evidence showing the harmful effects of SOPs on endothelial function.

28 citations

Journal ArticleDOI
TL;DR: In this paper, the authors reviewed the clinical characteristics of COVID-19 associated endothelial dysfunction and the likely pathological mechanisms underlying the disease including direct cell entry or indirect immune overreactions after SARS-CoV-2 infection.

28 citations

Patent
07 Apr 2009
TL;DR: In this article, the visibility of an object in a digital picture is enhanced by comparing an input video of the digital picture with stored information representative of the nature and characteristics of the object to develop object localization information that identifies and locates the object.
Abstract: The visibility of an object in a digital picture is enhanced by comparing an input video of the digital picture with stored information representative of the nature and characteristics of the object to develop object localization information that identifies and locates the object. The visibility of the object and the region in which the object is located is enhanced by image processing and the enhanced input video is encoded.

28 citations


Cited by
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08 Dec 2001-BMJ
TL;DR: There is, I think, something ethereal about i —the square root of minus one, which seems an odd beast at that time—an intruder hovering on the edge of reality.
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 …

33,785 citations

01 May 1993
TL;DR: 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.
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.

29,323 citations

28 Jul 2005
TL;DR: PfPMP1)与感染红细胞、树突状组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�ly.
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。

18,940 citations