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Search Results: 1 - 10 of 4211 matches for " Shiying Miao "
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Some Properties of the g-Good-Neighbor (g-Extra) Diagnosability of a Multiprocessor System  [PDF]
Yunxia Ren, Shiying Wang
American Journal of Computational Mathematics (AJCM) , 2016, DOI: 10.4236/ajcm.2016.63027
Abstract: Diagnosability of a multiprocessor system is one important study topic. In 2012, Peng et al. proposed a measure for fault tolerance of the system, which is called the g-good-neighbor diagnosability that restrains every fault-free node containing at least g fault-free neighbors. In 2015, Zhang et al. proposed a measure for fault diagnosis of the system, namely, g-extra diagnosability, which restrains that every fault-free component has at least g+1 fault-free nodes. In this paper, we obtain some properties of the g-good-neighbor (g-extra) diagnosability of the system and give the g-good-neighbor (g-extra) diagnosability of some graphs under the PMC model and MM* model.
The 2-Extra Diagnosability of Alternating Group Graphs under the PMC Model and MM* Model  [PDF]
Shiying Wang, Yunxia Ren
American Journal of Computational Mathematics (AJCM) , 2018, DOI: 10.4236/ajcm.2018.81004
Abstract: Diagnosability of a multiprocessor system is one important study topic. In 2015, Zhang et al. proposed a new measure for fault diagnosis of the system, namely, g-extra diagnosability, which restrains that every fault-free component has at least (g + 1) fault-free nodes. As a favorable topology structure of interconnection networks, the n-dimensional alternating group graph AGn has many good properties. In this paper, we give that the 2-extra diagnosability of AGn is 6n - 17 for n 5 under the PMC model and MM* model.
Exosome-Related Multi-Pass Transmembrane Protein TSAP6 Is a Target of Rhomboid Protease RHBDD1-Induced Proteolysis
Chunhua Wan, Jun Fu, Yong Wang, Shiying Miao, Wei Song, Linfang Wang
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0037452
Abstract: We have previously reported that rhomboid domain containing 1 (RHBDD1), a mammalian rhomboid protease highly expressed in the testis, can cleave the Bcl-2 protein Bik. In this study, we identified a multi-pass transmembrane protein, tumor suppressor activated pathway-6 (TSAP6) as a potential substrate of RHBDD1. RHBDD1 was found to induce the proteolysis of TSAP6 in a dose- and activity-dependent manner. The cleavage of TSAP6 was not restricted to its glycosylated form and occurred in three different regions. In addition, mass spectrometry and mutagenesis analyses both indicated that the major cleavage site laid in the C-terminal of the third transmembrane domain of TSAP6. A somatic cell knock-in approach was used to genetically inactivate the endogenous RHBDD1 in HCT116 and RKO colon cancer cells. Exosome secretion was significantly elevated when RHBDD1 was inactivated in the two cells lines. The increased exosome secretion was verfied through the detection of certain exosomal components, including Tsg101, Tf-R, FasL and Trail. In addition, the elevation of exosome secretion by RHBDD1 inactivation was reduced when TSAP6 was knocked down, indicating that the role of RHBDD1 in regulating exosomal trafficking is very likely to be TSAP6-dependent. We found that the increase in FasL and Trail increased exosome-induced apoptosis in Jurkat cells. Taken together, our findings suggest that RHBDD1 is involved in the regulation of a nonclassical exosomal secretion pathway through the restriction of TSAP6.
GC-1 mRHBDD1 knockdown spermatogonia cells lose their spermatogenic capacity in mouse seminiferous tubules
Yong Wang, Wei Song, Shuchun Li, Xin Guan, Shiying Miao, Shudong Zong, SS Koide, Linfang Wang
BMC Cell Biology , 2009, DOI: 10.1186/1471-2121-10-25
Abstract: Stable mRHBDD1 knockdown GC-1 cells were sensitive to apoptotic stimuli, PS341 and UV irradiation. In vitro, they survived and proliferated normally. However, they lost the ability to survive and differentiate in mouse seminiferous tubules.Our findings suggest that mRHBDD1 may be associated with mammalian spermatogenesis.Spermatogenesis generates functional sperm cells from initially undifferentiated germ cells. This involves the proliferation of spermatogonia, meiosis of spermatocytes and the differentiation of spermatids into spermatozoa. It is a complex developmental program in which myriad events take place to ensure that the germ cells reach their proper stages of development at the appropriate times. Normal spermatogenesis requires a well-regulated balance of several processes, including cell proliferation, differentiation and apoptosis.Apoptosis is a key phenomenon during spermatogenesis. For instance, an early, massive wave of germ cell apoptosis occurs at puberty. This event takes place during postnatal weeks 2 to 4 in mice, with a peak after 3 weeks [1-3]. It is estimated that 75% of spermatogenic cells undergo apoptosis during development [4,5], ensuring the maintenance of a critical ratio between maturing germ cells and Sertoli cells [2,6]. Sporadic apoptosis also occurs, primarily in spermatogonia and spermatocytes [2], eliminating defective germ cells with mutated DNA [7].The Rhomboid family comprises polytopic membrane proteins, which may be the most widely-conserved membrane proteins identified to date [8]. They share conserved biochemical properties in all biological kingdoms. Rhomboid proteases, which have been well studied in Drosophila, appear to regulate EGF receptor signalling pathways, thereby controlling growth and development [9,10]. In addition, some yeast Rhomboid proteases have been found to play important roles in mitochondrial membrane remodelling [11], while some parasite proteases containing a Rhomboid domain are important for invasiv
Small Kinetochore Associated Protein (SKAP) Promotes UV-Induced Cell Apoptosis through Negatively Regulating Pre-mRNA Processing Factor 19 (Prp19)
Shan Lu, Renxian Wang, Congli Cai, Junbo Liang, Longchang Xu, Shiying Miao, Linfang Wang, Wei Song
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0092712
Abstract: Apoptosis is a regulated cellular suicide program that is critical for the development and maintenance of healthy tissues. Previous studies have shown that small kinetochore associated protein (SKAP) cooperates with kinetochore and mitotic spindle proteins to regulate mitosis. However, the role of SKAP in apoptosis has not been investigated. We have identified a new interaction involving SKAP, and we propose a mechanism through which SKAP regulates cell apoptosis. Our experiments demonstrate that both overexpression and knockdown of SKAP sensitize cells to UV-induced apoptosis. Further study has revealed that SKAP interacts with Pre-mRNA processing Factor 19 (Prp19). We find that UV-induced apoptosis can be inhibited by ectopic expression of Prp19, whereas silencing Prp19 has the opposite effect. Additionally, SKAP negatively regulates the protein levels of Prp19, whereas Prp19 does not alter SKAP expression. Finally, rescue experiments demonstrate that the pro-apoptotic role of SKAP is executed through Prp19. Taken together, these findings suggest that SKAP promotes UV-induced cell apoptosis by negatively regulating the anti-apoptotic protein Prp19.
The Protective Effect of Bcl-xl Overexpression against Oxidative Stress-Induced Vascular Endothelial Cell Injury and the Role of the Akt/eNOS Pathway
Leng Ni,Tianjia Li,Bao Liu,Xitao Song,Genhuan Yang,Linfang Wang,Shiying Miao,Changwei Liu
International Journal of Molecular Sciences , 2013, DOI: 10.3390/ijms141122149
Abstract: Restenosis after intraluminal or open vascular reconstruction remains an important clinical problem. Vascular endothelial cell (EC) injury induced by oxidative stress plays an important role in the development of intimal hyperplasia. In this study, we sought to evaluate the protective effects of Bcl-xl overexpression in vitro on oxidative stress-induced EC injury and the role of the Akt/endothelial nitric oxide synthase (eNOS) pathway. Human umbilical vein endothelial cells (HUVECs) exposed to hydrogen peroxide (H 2O 2, 0.5 mM) were used as the experimental oxidative stress model. The Bcl-xl gene was transferred into HUVECs through recombinant adenovirus vector pAdxsi-GFP- Bcl-xl before oxidative treatment. Cell apoptosis was evaluated by Annexin V/propidium iodide and Hoechst staining, caspase-7 and PARP cleavage. Cell viability was assessed using the cell counting kit-8 assay, proliferating cell nuclear antigen (PCNA) immunocytochemical detection and the scratching assay. Expressions of Akt, phospho-Akt and eNOS were detected by Western blotting. Our results showed that H 2O 2 induced apoptosis and decreased the cell viability of HUVECs. Bcl-xl overexpression significantly protected cells from H 2O 2-induced cell damage and apoptosis and maintained the cell function. Furthermore, the level of phospho-Akt and eNOS protein expression was significantly elevated when pretreated with Bcl-xl gene transferring. These findings suggest that Bcl-xl overexpression exerts an anti-apoptotic and protective effect on EC function. The Akt/eNOS signaling pathway is probably involved in these processes.
Dissolution of Expanded Polystyrene in Cycloalkane Solutions  [PDF]
Shiying Tao, Boyang Li, Hui Huang
Open Journal of Applied Sciences (OJAppS) , 2018, DOI: 10.4236/ojapps.2018.810037
Abstract: Feasibility of dissolution and utilization of expanded polystyrene in cycloalkane solutions was investigated in this work. The dissolution process of expanded polystyrene in several cycloalkane solutions decalin, cyclohexane and methyl cyclohexane was studied. The effect of dissolution temperature, mechanical agitation, ultrasonic wave and stirring rate was studied under optimized conditions. Mass transfer coefficients were fitted. The results showed that the dissolution rate of expanded polystyrene in different cycloalkane solutions was ranked as decalin > methyl cyclohexane > cyclohexane; higher dissolution temperature and faster stirring rate could speed up the dissolution of expanded polystyrene; the effect of mechanical agitation was superior to ultrasonic condition; the solubility of top face was better than side face and under face.
Lysine-Specific Demethylase 1 (LSD1/KDM1A) Contributes to Colorectal Tumorigenesis via Activation of the Wnt/Β-Catenin Pathway by Down-Regulating Dickkopf-1 (DKK1)
Zebin Huang, Shangze Li, Wei Song, Xin Li, Qinshan Li, Zeyan Zhang, Yongqing Han, Xiaodong Zhang, Shiying Miao, Runlei Du, Linfang Wang
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0070077
Abstract: We collected paired samples of tumor and adjacent normal colorectal tissues from 22 patients with colorectal carcinoma to compare the differences in the expression of lysine specific demethylase 1 (LSD1) in these two tissues. The results showed that in 19 paired samples (86.4%), LSD1 is more highly expressed in tumor tissue than in normal tissue. To explore the role of LSD1 in colorectal tumorigenesis, we used somatic cell gene targeting to generate an LSD1 knockout (KO) HCT 116 human colorectal cancer cell line as a research model. The analysis of phenotypic changes showed that LSD1 KO colorectal cancer cells are less tumorigenic, both in vivo and in vitro. The differential expression analysis of the cells by mRNA sequencing (RNA-Seq) yielded 2,663 differentially expressed genes, and 28 of these genes had highly significant differences (Q <0.01). We then selected the 4 colorectal cancer-related genes ADM, DKK1, HAS3 and SMURF2 for quantitative real-time PCR verification. The results showed that the differences in the expression of ADM, DKK1 and HAS3 were consistent with those measured using the RNA-Seq data. As DKK1 was the gene with the most significant differential expression, we analyzed the key proteins of the DKK1-related Wnt/β-catenin signaling pathway and found that, after knocking out LSD1, the amount of free β-catenin translocated to the nucleus was significantly reduced and that the transcription of the signaling pathway target gene c-Myc was down-regulated. Our studies show that LSD1 activates the Wnt/β-catenin signaling pathway by down-regulating the pathway antagonist DKK1, which may be one of the mechanisms leading to colorectal tumorigenesis.
Doing Right: A Practical Guide to Ethics for Medical Trainees and Physicians
Shiying Liu,Anthony So
University of Toronto Medical Journal , 2009, DOI: 10.5015/utmj.v86i3.386
A Proof for g-Good-Neighbor Diagnosability of Exchanged Hypercubes  [PDF]
Yunxia Ren, Shiying Wang
American Journal of Computational Mathematics (AJCM) , 2019, DOI: 10.4236/ajcm.2019.93010
The diagnosability of a multiprocessor system or an interconnection network is an important research topic. The system and an interconnection network have an underlying topology, which is usually presented by a graph. In this paper, we show proof for the g-good-neighbor diagnosability of the exchanged hypercube EH (s,t) under the PMC model and MM* model.
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