Difference and Enlightenment of Livelihood Policies Between China and the United Sates

This paper analyzes and summarizes the American livelihood policy on the basis of educational public policy, medicine and health public policy, employment and entrepreneurship public policy and compulsory education public policy four policies; learns some experiences and shortages of American livelihood policy. Based on above analyses, putting forward some enlightenments and experiences of China livelihood policy

Comparison and Reference of Public Policy on People’s Livelihood Between China and the United Sates—Based on the Case of Chongqing

Education, health care, employment, social security and other livelihood policies related to people’s vital interests and social harmony and stability, China and the U.S. government attach great importance to the formulation and improvement of people’s livelihood policies. However, due to the different political systems, economic, social, cultural and other aspects between the two countries, the livelihood policies of the two countries are quite different too. Based on a brief introduction of livelihood policies of China and U.S., on the comparative analysis of the livelihood policies differences between the two countries, noting that the significant difference between China and U.S. Livelihood policies is that the market-oriented and government-led, while the laws and regulations completeness and the guidance services of policy also have a large gap. Combined Chongqing practice, Chongqing need to learn from U.S. in formulating and improving the livelihood policies, market, social policy- oriented of livelihood, while the people’s livelihood policy system, guidance and services and integration of urban-rural livelihood policies also need to improve constantly. Key words: People’s livelihood policy; China and the U.S.; Comparison; Referenc

Deconstructing Survivin: comprehensive genetic analysis of Survivin function by conditional knockout in a vertebrate cell line

Survivin is a key cellular protein thought to function in apoptotic regulation, mitotic progression, or possibly both. In this study, we describe the isolation of two conditional knockouts of the survivin gene in chicken DT40 cells. DT40 cells lacking Survivin die in interphase after failing to complete cytokinesis. However, these cells show normal sensitivity to the chemotherapeutic agent etoposide. Expression of Survivin mutants against a null background to reassess the role of several key residues reveals that DT40 cells can grow normally if their sole Survivin is missing a widely studied cyclin-dependent kinase phosphorylation site or sites reportedly essential for binding to Smac or aurora B. Mutations in the nuclear export sequence or dimerization interface render cells temperature sensitive for growth. As an important caveat for other studies in which protein function is studied by transient transfection, three of the Survivin mutants fail to localize in the presence of the wild-type protein but do localize and indeed support life in its absence

Use of D140 conditional-knockout cell lines to study chromosomal passenger protein function

The chromosomal passenger complex (CPC-INCENP, Aurora B kinase, Survivin and Borealin) is implicated in many mitotic processes. Here we describe how we generated DT40 conditional knockout cell lines for incenp1 and survivin1 to better understand the role of these CPC subunits in the control of Aurora B kinase activity. These lines enabled us to reassess current knowledge of Survivin function and to show that INCENP acts as a rheostat for Aurora B activity

Protective Effect of Optic Atrophy 1 on Cardiomyocyte Oxidative Stress: Roles of Mitophagy, Mitochondrial Fission, and MAPK/ERK Signaling

Myocardial infarction is associated with oxidative stress and mitochondrial damage. However, the regulatory mechanisms underlying cardiomyocyte oxidative stress during myocardial infarction are not fully understood. In the present study, we explored the cardioprotective action of optic atrophy 1- (Opa1-) mediated mitochondrial autophagy (mitophagy) in oxidative stress-challenged cardiomyocytes, with a focus on mitochondrial homeostasis and the MAPK/ERK pathway. Our results demonstrated that overexpression of Opa1 in cultured rat H9C2 cardiomyocytes, a procedure that stimulates mitophagy, attenuates oxidative stress and increases cellular antioxidant capacity. Activation of Opa1-mediated mitophagy suppressed cardiomyocyte apoptosis by downregulating Bax, caspase-9, and caspase-12 and upregulating Bcl-2 and c-IAP. Using mitochondrial tracker staining and a reactive oxygen species indicator, our assays showed that Opa1-mediated mitophagy attenuated mitochondrial fission and reduced ROS production in cardiomyocytes. In addition, we found that inhibition of the MAPK/ERK pathway abolished the antioxidant action of Opa1-mediated mitophagy in these cells. Taken together, our data demonstrate that Opa1-mediated mitophagy protects cardiomyocytes against oxidative stress damage through inhibition of mitochondrial fission and activation of MAPK/ERK signaling. These findings reveal a critical role for Opa1 in the modulation of cardiomyocyte redox balance and suggest a potential target for the treatment of myocardial infarction