Towards Perpetual Peace: Kant and Rawls

( Hong Mei Qu ) 한국윤리학회 2013 倫理硏究 Vol.89 No.1

In 1795, Kant, as a philosopher who never left his hometown published the famous Perpetual Peace which is about the future of all human beings. What dazzled us in the short article are not the concrete strategies for ending war, but the philosophical principles on which a just and lasting world peace can be based. It is this kind of philosophical sketch for perpetual peace that influences us descendants so much. Two hundred years later, Rawls finished The Law of Peoples, in which he expresses the same hope and belief with Kant: perpetual peace for human beings. Rawls himself also indicates that his thought on the principle of the Law of Peoples is based on Kant`s ideal on the world federation.1 However, after reading the two books, I find that Rawls does not follow the train of Kantian thought in the Perpetual Peace as he claims. In order to support this idea, firstly, I refer to Kantian cosmopolitanism which in my opinion is the original mode of all kinds of theories on contemporary global justice. In the second part, I speak of Rawls`s theory on global justice in The Law of Peoples which is in fact describing a hierarchy of different communities and states for us. In the third and fourth parts, I argue that Kantian thought is not only more theoretically far-reaching but also practically viable than Rawls`s by comparing them from the basis of their theories.

Ischemic postconditioning protects cardiomyocytes against ischemia/reperfusion injury by inducing MIP2

Hong-Lin Zhu,Kang-Kai Wang,Xing Wei,Shun-Lin Qu,Chi Zhang,Xiao-Xia Zuo,Yan-Sheng Feng,Qi Luo,Guang-Wen Chen,Mei-Dong Liu,Lei Jiang,Xian-Zhong Xiao 생화학분자생물학회 2011 Experimental and molecular medicine Vol.43 No.8

Cardiomyocytes can resist ischemia/reperfusion (I/R)injury through ischemic postconditioning (IPoC)which is repetitive ischemia induced during the onset of reperfusion. Myocardial ischemic preconditioning up-regulated protein 2 (MIP2) is a member of the WD-40family proteins, we previously showed that MIP2 was up-regulated during ischemic preconditioning (IPC). As IPC and IPoC engaged similar molecular mechanisms in cardioprotection, this study aimed to elucidate whether MIP2 was up-regulated during IPoC and contributed to IPoC-mediated protection against I/R injury. The experiment was conducted on two models,an in vivo open chest rat coronary artery occlusion model and an in vitro model with H9c2 myogenic cells. In both models, 3 groups were constituted and randomly designated as the sham, I/R and IPoC/hypoxia postconditioning (HPoC) groups. In the IPoC group, after 45 min of ischemia, hearts were allowed three cycles of reperfusion/ischemia phases (each of 30 s duration)followed by reperfusion. In the HPoC group, after 6 h of hypoxia, H9c2 cells were subjected to three cycles of 10 minute reoxygenation and 10 minute hypoxia followed by reoxygenation. IPoC significantly reduced the infarct size, plasma level of Lactate dehydrogenase and creatine kinase MB in rats. 12 h after the reperfusion,MIP2 mRNA levels in the IPoC group were 10 folds that of the sham group and 1.4 folds that of the I/R group. Increased expression of MIP2 mRNA and attenuation of apoptosis were similarly observed in the HPoC group in the in vitro model. These effects were blunted by transfection with MIP2 siRNA in the H9c2cells. This study demonstrated that IPoC induced protection was associated with increased expression of MIP2. Both MIP2 overexpression and MIP2 suppression can influence the IPoC induced protection.

Asparagine Residue at Position 71 is Responsible for Alkali - Tolerance of the Xylanase from Bacillus pumilus A - 30

(Xiang Mei Liu),(Meng Qi),(Jian Qiang Lin),(Zhi Hong Wu),(Yin Bo Qu) 한국미생물생명공학회 2001 Journal of microbiology and biotechnology Vol.11 No.3

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Ischemic postconditioning protects cardiomyocytes against ischemia/reperfusion injury by inducing MIP2

Zhu, Hong-Lin,Wei, Xing,Qu, Shun-Lin,Zhang, Chi,Zuo, Xiao-Xia,Feng, Yan-Sheng,Luo, Qi,Chen, Guang-Wen,Liu, Mei-Dong,Jiang, Lei,Xiao, Xian-Zhong,Wang, Kang-Kai Korean Society for Biochemistry and Molecular Bion 2011 Experimental and molecular medicine Vol.43 No.8

Cardiomyocytes can resist ischemia/reperfusion(I/R) injury through ischemic postconditioning (IPoC) which is repetitive ischemia induced during the onset of reperfusion. Myocardial ischemic preconditioning up-regulated protein 2 (MIP2) is a member of the WD-40 family proteins, we previously showed that MIP2 was up-regulated during ischemic preconditioning (IPC). As IPC and IPoC engaged similar molecular mechanisms in cardioprotection, this study aimed to elucidate whether MIP2 was up-regulated during IPoC and contributed to IPoC-mediated protection against I/R injury. The experiment was conducted on two models, an $in$ $vivo$ open chest rat coronary artery occlusion model and an $in$ $vitro$ model with H9c2 myogenic cells. In both models, 3 groups were constituted and randomly designated as the sham, I/R and IPoC/hypoxia postconditioning (HPoC) groups. In the IPoC group, after 45 min of ischemia, hearts were allowed three cycles of reperfusion/ischemia phases (each of 30 s duration) followed by reperfusion. In the HPoC group, after 6 h of hypoxia, H9c2 cells were subjected to three cycles of 10 minute reoxygenation and 10 minute hypoxia followed by reoxygenation. IPoC significantly reduced the infarct size, plasma level of Lactate dehydrogenase and creatine kinase MB in rats. 12 h after the reperfusion, MIP2 mRNA levels in the IPoC group were 10 folds that of the sham group and 1.4 folds that of the I/R group. Increased expression of MIP2 mRNA and attenuation of apoptosis were similarly observed in the HPoC group in the $in$ $vitro$ model. These effects were blunted by transfection with MIP2 siRNA in the H9c2 cells. This study demonstrated that IPoC induced protection was associated with increased expression of MIP2. Both MIP2 overexpression and MIP2 suppression can influence the IPoC induced protection.

Spurious mode distinguish by eigensystem realization algorithm with improved stabilization diagram

Chun-Xu Qu,Ting-Hua Yi,Xiao-Mei Yang,Hong-Nan Li 국제구조공학회 2017 Structural Engineering and Mechanics, An Int'l Jou Vol.63 No.6

Modal parameter identification plays a key role in the structural health monitoring (SHM) for civil engineering. Eigensystem realization algorithm (ERA) is one of the most popular identification methods. However, the complex environment around civil structures can introduce the noises into the measurement from SHM system. The spurious modes would be generated due to the noises during ERA process, which are usually ignored and be recognized as physical modes. This paper proposes an improved stabilization diagram method in ERA to distinguish the spurious modes. First, it is proved that the ERA can be performed by any two Hankel matrices with one time step shift. The effect of noises on the eigenvalues of structure is illustrated when the choice of two Hankel matrices with one time step shift is different. Then, a moving data diagram is proposed to combine the traditional stabilization diagram to form the improved stabilization diagram method. The moving data diagram shows the mode variation along the different choice of Hankel matrices, which indicates whether the mode is spurious or not. The traditional stabilization diagram helps to determine the concerned truncated order before moving data diagram is implemented. Finally, the proposed method is proved through a numerical example. The results show that the proposed method can distinguish the spurious modes.

Isolation and Characterization of Bacillus sp. Producing Broad-Spectrum Antibiotics Against Human and Plant Pathogenic Fungi

( Na Chen ),( Min Jin ),( Hong Mei Qu ),( Zhi Qiang Chen ),( Zhao Li Chen ),( Zhi Gang Qiu ),( Xin Wei Wang ),( Jun Wen Li ) 한국미생물 · 생명공학회 2012 Journal of microbiology and biotechnology Vol.22 No.2

A strain of bacterium producing antifungal antibiotic was isolated and identification of the strain was attempted. We could identify the bacterium as being a Bacillus sp., based on morphological observation, physiological characteristics, and 16S rDNA sequence analysis, thus leading us to designate the strain as Bacillus sp. AH-E-1. The strain showed potent antibiotic activity against phytopathogenic and human pathogenic fungi by inducing mycelial distortion and swelling and inhibiting spore germination. The antibiotic metabolite produced by the strain demonstrated excellent thermal and pH (2-11) stability, but was labile to autoclaving. From these results, we could find a broader antifungal activity of Bacillus genus. Isolation and characterization of the active agent produced by the strain are under progress.

IGF-1 from Adipose-Derived Mesenchymal Stem Cells Promotes Radioresistance of Breast Cancer Cells

Yang, Hui-Ying,Qu, Rong-Mei,Lin, Xiao-Shan,Liu, Tong-Xin,Sun, Quan-Quan,Yang, Chun,Li, Xiao-Hong,Lu, Wei,Hu, Xiao-Fang,Dai, Jing-Xing,Yuan, Lin Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.23

Purpose: The aim of this study was to investigate effects of adipose-derived mesenchymal stem cells (AMSCs) on radioresistance of breast cancer cells. Materials and Methods: MTT assays were used to detect any influence of AMSC supernatants on proliferation of breast cancer cells; cell migration assays were used to determine the effect of breast cancer cells on the recruitment of AMSCs; the cell survival fraction post-irradiation was assessed by clonogenic survival assay; ${\gamma}$-H2AX foci number post-irradiation was determined via fluorescence microscopy; and expression of IGF-1R was detected by Western blotting. Results: AMSC supernatants promoted proliferation and radioresistance of breast cancer cells. Breast cancer cells could recruit AMSCs, especially after irradiation. IGF-1 derived from AMSCs might be responsible for the radioresistance of breast cancer cells. Conclusions: Our results suggest that AMSCs in the tumor microenvironment may affect the outcome of radiotherapy for breast cancer in vitro.

Prognostic Impact of Elevation of Vascular Endothelial Growth Factor Family Expression in Patients with Non-small Cell lung Cancer: an Updated Meta-analysis

Zheng, Chun-Long,Qiu, Chen,Shen, Mei-Xiao,Qu, Xiao,Zhang, Tie-Hong,Zhang, Ji-Hong,Du, Jia-Jun Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.5

Background: The vascular endothelial growth factor family has been implicated in tumorigenesis and metastasis. The prognostic value of each vascular endothelial growth factor family member, particular VEGF/VEGFR co-expression, in patients with non-small lung cancer remains controversial. Materials and Methods: Relevant literature was identified by searching PubMed, EMBASE and Web of Science. Studies evaluating expression of VEGFs and/or VEGFRs by immunohistochemistry or ELISA in lung cancer tissue were eligible for inclusion. Hazard ratios (HRs) and 95% confidence intervals (CIs) from individual study were pooled by using a fixed- or random-effect model, heterogeneity and publication bias analyses were also performed. Results: 74 studies covering 7,631 patients were included in the meta-analysis. Regarding pro-angiogenesis factors, the expression of VEGFA (HR=1.633, 95%CI: 1.490-1.791) and VEGFR1 (HR=1.924, 95%CI: 1.220-3.034) was associated separately with poor survival. Especially, VEGFA over-expression was an independent prognostic factor in adenocarcinoma (ADC) (HR=1.775, 95%CI: 1.384-2.275) and SCC (HR=2.919, 95%CI: 2.060-4.137). Co-expression of VEGFA/VEGFR2 (HR=2.011, 95%CI: 1.405-2.876) was also significantly associated with worse survival. For lymphangiogenesis factors, the expression of VEGFC (HR=1.611, 95%CI: 1.407-1.844) predicted a poor prognosis. Co-expression of VEGFC/VEGFR3 (HR=2.436, 95%CI: 1.468-4.043) emerged as a preferable prognostic marker. Conclusions: The expression of VEGFA (particularly in SCC and early stage NSCLC), VEGFC, VEGFR1 indicates separately an unfavorable prognosis in patients with NSCLC. Co-expression VEGFA/VEGFR2 is comparable with VEGFC/VEGFR3, both featuring sufficient discrimination value as preferable as prognostic biologic markers.