http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Hazari, Arnab,Fu Chen Hsiao,Lifan Yan,Junseok Heo,Millunchick, Joanna Mirecki,Dallesasse, John M.,Bhattacharya, Pallab IEEE 2017 IEEE journal of quantum electronics Vol.53 No.4
<P>A feasible optical interconnect on a silicon complementary metal-oxide-semiconductor chip demands epitaxial growth and monolithic integration of diode lasers and optical detectors with guided wave components on a (001) Si wafer, with all the components preferably operating in the wavelength range of 1.3-1.55 μm at room temperature. It is also desirable for the fabrication technique to be relatively simple and reproducible. Techniques demonstrated in the past for having optically and electrically pumped GaAs and InP-based lasers on silicon include wafer bonding, selective area epitaxy, epitaxy on tilted substrates, and use of quantum dot or planar buffer layers. Here, we present a novel monolithic optical interconnect on a (001) Si substrate consisting of a III-nitride dot-in-nanowire array edge emitting diode laser and guided wave photodiode, with a planar SiO<SUB>2</SUB>/Si<SUB>3</SUB>N<SUB>4</SUB> dielectric waveguide in between. The active devices are realized with the same nanowire heterostructure by one-step epitaxy. The electronic properties of the InN dot-like nanostructures and mode confinement and propagation in the nanowire waveguides have been modeled. The laser, emitting at the desired wavelength of 1.3 μm, with threshold current ~350 mA for a device of dimension 50 μm × 2 mm, has been characterized in detail. The detector exhibits a responsivity ~0.1 A/W at 1.3 μm. Operation of the entire optical interconnect via the dielectric waveguide is demonstrated.</P>
Matricellular Protein CCN5 Reverses Established Cardiac Fibrosis
Jeong, Dongtak,Lee, Min-Ah,Li, Yan,Yang, Dong Kwon,Kho, Changwon,Oh, Jae Gyun,Hong, Gyeongdeok,Lee, Ahyoung,Song, Min Ho,LaRocca, Thomas J.,Chen, Jiqiu,Liang, Lifan,Mitsuyama, Shinichi,D'Escamard, Val American College of Cardiology 2016 Journal of the American College of Cardiology Vol.67 No.13
<P><B>Abstract</B></P><P><B>Background</B></P><P>Cardiac fibrosis (CF) is associated with increased ventricular stiffness and diastolic dysfunction and is an independent predictor of long-term clinical outcomes of patients with heart failure (HF). We previously showed that the matricellular CCN5 protein is cardioprotective via its ability to inhibit CF and preserve cardiac contractility.</P><P><B>Objectives</B></P><P>This study examined the role of CCN5 in human heart failure and tested whether CCN5 can reverse established CF in an experimental model of HF induced by pressure overload.</P><P><B>Methods</B></P><P>Human hearts were obtained from patients with end-stage heart failure. Extensive CF was induced by applying transverse aortic constriction for 8 weeks, which was followed by adeno-associated virus-mediated transfer of CCN5 to the heart. Eight weeks following gene transfer, cellular and molecular effects were examined.</P><P><B>Results</B></P><P>Expression of CCN5 was significantly decreased in failing hearts from patients with end-stage heart failure compared to nonfailing hearts. Trichrome staining and myofibroblast content measurements revealed that the established CF had been reversed by CCN5 gene transfer. Anti-CF effects of CCN5 were associated with inhibition of the transforming growth factor beta signaling pathway. CCN5 significantly inhibited endothelial-mesenchymal transition and fibroblast-to-myofibroblast transdifferentiation, which are 2 critical processes for CF progression, both in vivo and in vitro. In addition, CCN5 induced apoptosis in myofibroblasts, but not in cardiomyocytes or fibroblasts, both in vivo and in vitro. CCN5 provoked the intrinsic apoptotic pathway specifically in myofibroblasts, which may have been due the ability of CCN5 to inhibit the activity of NFκB, an antiapoptotic molecule.</P><P><B>Conclusions</B></P><P>CCN5 can reverse established CF by inhibiting the generation of and enhancing apoptosis of myofibroblasts in the myocardium. CCN5 may provide a novel platform for the development of targeted anti-CF therapies.</P>