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OFEX Controller to Improve Queueing and User Performance in Multi-bottleneck Networks
Jungang Liu,Oliver W.W. Yang 한국전자통신연구원 2014 ETRI Journal Vol.36 No.3
We have designed and investigated a new congestioncontrol scheme, called optimal and fully explicit (OFEX)controller. Different from existing relatively explicitcontrollers, this new scheme can provide not only optimalbandwidth allocation but also a fully explicit congestionsignal to sources. It uses the congestion signal from themost congested link instead of the cumulative signal fromthe flow path. In this way, it overcomes the drawback ofrelatively explicit controllers exhibiting bias toward multibottleneckedusers and significantly improves theirconvergence speed and source throughput performance. Furthermore, our OFEX-controller design considers adynamic model by proposing a remedial measure againstthe unpredictable bandwidth changes in contention-basedmulti-access networks. Compared with formerworks/controllers, this remedy also effectively reduces theinstantaneous queue size in a router and thus significantlyimproves queuing delay and packet loss performance. Wehave evaluated the effectiveness of the OFEX controller inOPNET. The experimental comparison with the existingrelatively explicit controllers verifies the superiority of ournew scheme.
PICOT Inhibits Cardiac Hypertrophy and Enhances Ventricular Function and Cardiomyocyte Contractility
Jeong, Dongtak,Cha, Hyeseon,Kim, Eunyoung,Kang, Misuk,Yang, Dong Kwon,Kim, Ji Myoung,Yoon, Pyoung Oh,Oh, Jae Gyun,Bernecker, Oliver Y.,Sakata, Susumu,Thu, Le Thi,Cui, Lei,Lee, Young-Hoon,Kim, Do Han,W Grune & Stratton 2006 Circulation research Vol.99 No.3
<P>Multiple signaling pathways involving protein kinase C (PKC) have been implicated in the development of cardiac hypertrophy. We observed that a putative PKC inhibitor, PICOT (PKC-Interacting Cousin Of Thioredoxin) was upregulated in response to hypertrophic stimuli both in vitro and in vivo. This suggested that PICOT may act as an endogenous negative feedback regulator of cardiac hypertrophy through its ability to inhibit PKC activity, which is elevated during cardiac hypertrophy. Adenovirus-mediated gene transfer of PICOT completely blocked the hypertrophic response of neonatal rat cardiomyocytes to enthothelin-1 and phenylephrine, as demonstrated by cell size, sarcomere rearrangement, atrial natriuretic factor expression, and rates of protein synthesis. Transgenic mice with cardiac-specific overexpression of PICOT showed that PICOT is a potent inhibitor of cardiac hypertrophy induced by pressure overload. In addition, PICOT overexpression dramatically increased the ventricular function and cardiomyocyte contractility as measured by ejection fraction and end-systolic pressure of transgenic hearts and peak shortening of isolated cardiomyocytes, respectively. Intracellular Ca(2+) handing analysis revealed that increases in myofilament Ca(2+) responsiveness, together with increased rate of sarcoplasmic reticulum Ca(2+) reuptake, are associated with the enhanced contractility in PICOT-overexpressing cardiomyocytes. The inhibition of cardiac remodeling by of PICOT with a concomitant increase in ventricular function and cardiomyocyte contractility suggests that PICOT may provide an efficient modality for treatment of cardiac hypertrophy and heart failure.</P>