http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
An Extension to TCP HACK for Improving the Performance of TCP in Lossy Environments
Ying Xia Niu,Choong Seon Hong 한국정보과학회 2002 한국정보과학회 학술발표논문집 Vol.29 No.1A
TCP has been designed and tuned as a reliable transfer protocol for wired links. However, it incurs end-to-end performance degradation in wireless environments where packet loss is very high. TCP HACK(Header Checksum Option) is a novel mechanism proposed to improve original TCP in lossy link. It presents an extension to TCP that enables TCP to distinguish packet corruption from congestion in losssy environments. TCP HACK performs well when the sender receives the special ACKs correctly, but if the ACKs are also lost much, the efficient of TCP HACK will not be prominent. In this paper we present an extension to TCP HACK, which can perform well even when the ACKs are much corrupted.
Niu, Ying-Jie,Zhou, Dongjie,Zhou, Wenjun,Nie, Zheng-Wen,Kim, Ju-Yeon,Oh, YoungJin,Lee, So-Rim,Cui, Xiang-Shun The Korean Society of Animal Reproduction and Biot 2020 한국동물생명공학회지 Vol.35 No.1
Nitric oxide (NO)-induced protein S-nitrosylation triggers mitochondrial dysfunction and was related to cell senescence. However, the exact mechanism of these damages is not clear. In the present study, to investigate the relationship between in vitro aging and NO-induced protein S-nitrosylation, oocytes were treated with sodium nitroprusside dihydrate (SNP), and the resultant S-nitrosylated proteins were detected through biotin-switch assay. The results showed that levels of protein S-nitroso thiols (SNO)s and expression of S-nitrosoglutathione reductase (GSNOR) increased, while activity and function of mitochondria were impaired during oocyte aging. Addition of SNP, a NO donor, to the oocyte culture led to accelerated oocyte aging, increased mitochondrial dysfunction and damage, apoptosis, ATP deficiency, and enhanced ROS production. These results suggested that the increased NO signal during oocyte aging in vitro, accelerated oocyte degradation due to increased protein S-nitrosylation, and ROS-related redox signaling.
Melatonin enhances mitochondrial biogenesis and function in porcine preimplantation embryos
Ying-Jie Niu,Wenjun Zhou,Zheng-Wen Nie,Kyung-Tae Shin,Yong-Han Kim,Xiang-Shun Cui 한국수정란이식학회 2018 한국수정란이식학회 학술대회 Vol.2018 No.11
Melatonin (N-aceyl-5-methoxytryptamine) is the major hormone of the pineal gland. Melatonin and its metabolic derivatives possess extensive free-radical scavenging abilities and played critical roles in antioxidative stress, resisting apoptotic cell death. Melatonin also could enhance mitochondrial biogenesis in rats with carbon tetrachloride-induced liver fibrosis. In addition, melatonin attenuates myocardial ischemia/reperfusion injury by reducing oxidative stress damage via activation of SIRT1 signaling in a melatonin receptor 2-dependent manner. Activation or overexpression of SIRT1 could enhance mitochondrial biogenesis and function by inducing PGC-1α expression and deacetylation. The aim of this study was to investigate if melatonin enhances mitochondrial biogenesis and function via activation of melatonin receptor 2/SIRT1/PGC1-α Pathway. The results showed that Melatonin rescued rotenone-induced impairment of porcine embryo development. Treatment with rotenone could increase oxidative stress and apoptosis. Rotenone impaired mitochondrial functions by disrupting mitochondrial membrane potential, reducing mitochondrial DNA copy number and ATP production. Melatonin could improve SIRT1 and PGC-1α expression, inducing mitochondrial biogenesis. Rotenone-induced mitochondrial dysfunction and ATP deficiency was rescued by melatonin treatment, the oxidative stress and apoptosis was significantly decreased. Inhibition of melatonin receptor 2 or Knockdown of SIRT1 abolished the protective effects of melatonin on rotenone-induced impairments. Therefore, melatonin enhanced mitochondrial biogenesis and function, protected against rotenone-induced impairments.
Ying-Jie Niu,Dongjie Zhou,Wenjun Zhou,Zheng-Wen Nie,Ju-Yeon Kim,YoungJin Oh,So-Rim Lee,Xiang-Shun Cui 한국동물생명공학회(구 한국동물번식학회) 2020 Journal of Animal Reproduction and Biotechnology Vol.35 No.1
Nitric oxide (NO)-induced protein S-nitrosylation triggers mitochondrial dysfunction and was related to cell senescence. However, the exact mechanism of these damages is not clear. In the present study, to investigate the relationship between in vitro aging and NO-induced protein S-nitrosylation, oocytes were treated with sodium nitroprusside dihydrate (SNP), and the resultant S-nitrosylated proteins were detected through biotin-switch assay. The results showed that levels of protein S-nitroso thiols (SNO)s and expression of S-nitrosoglutathione reductase (GSNOR) increased, while activity and function of mitochondria were impaired during oocyte aging. Addition of SNP, a NO donor, to the oocyte culture led to accelerated oocyte aging, increased mitochondrial dysfunction and damage, apoptosis, ATP deficiency, and enhanced ROS production. These results suggested that the increased NO signal during oocyte aging in vitro, accelerated oocyte degradation due to increased protein S-nitrosylation, and ROS-related redox signaling.
Protective Effects of C-phycocyanin on Developmental Competence of Pig Parthenotes
Ying-Jie Niu,Jing Guo,Kyung-Tae Shin,Nam-Hyung Kim,Xiang-Shun Cui 한국동물생명공학회(구 한국동물번식학회) 2017 Reproductive & Developmental Biology(Supplement) Vol.41 No.2
C-phycocyanin (C-PC) is a biliprotein enriched in blue-green algae that is known to possess antioxidant, antiapoptosis, anti-inflammatory, and radical-scavenging properties in somatic cells. But the protective effect of C-PC on porcine embryo developmental competence in in vitro is little known. In the present study, we investigated the effect of C-PC on the development of porcine early embryos as well as the underlying its mechanisms. Different concentrations of C-CP (1, 2, 5, 8, 10 μg/mL) was added to the porcine zygote medium 5 (PZM-5) during in vitro culture. The results showed that 5 μg /mL C-PC significantly increased blastocyst formation. Blastocyst formation and its quality were significantly increased in 50 μM H2O2 treatment group following 5 μg/mL C-PC addition. C-PC prevented H2O2-induced compromise of mitochondrial membrane potential, release of cytochrome c from the mitochondria and reactive oxygen species generation. Furthermore, apoptosis, DNA damage level and autophagy in the blastocysts were attenuated by supplement of C-PC in H2O2-induced oxidative injury group compared with control. Taken together, these results suggest that C-PC has beneficial effects on the development of porcine parthenotes by attenuating mitochondrial dysfunction and oxidative stress.