Automatic Recognition of Seismic Intensity Based on RS and GIS: A Case Study in Wenchuan Ms8.0 Earthquake of China

In recent years, earthquakes have frequently occurred all over the world, which caused huge casualties and economic losses. It is very necessary and urgent to obtain the seismic intensity map timely so as to master the distribution of the disaster and provide supports for quick earthquake relief. Compared with traditional methods of drawing seismic intensity map, which require many investigations in the field of earthquake area or are too dependent on the empirical formulas, spatial information technologies such as Remote Sensing (RS) and Geographical Information System (GIS) can provide fast and economical way to automatically recognize the seismic intensity. With the integrated application of RS and GIS, this paper proposes a RS/GIS-based approach for automatic recognition of seismic intensity, in which RS is used to retrieve and extract the information on damages caused by earthquake, and GIS is applied to manage and display the data of seismic intensity. The case study in Wenchuan Ms8.0 earthquake in China shows that the information on seismic intensity can be automatically extracted from remotely sensed images as quickly as possible after earthquake occurrence, and the Digital Intensity Model (DIM) can be used to visually query and display the distribution of seismic intensity

c-Jun NH2-terminal Kinase Promotes Apoptosis by Down-Regulating the Transcriptional Co-repressor CtBP

Genetic knock out of the transcriptional co-repressor carboxyl-terminal-binding protein (CtBP) in mouse embryonic fibroblasts results in up-regulation of several genes involved in apoptosis. We predicted, therefore, that a propensity toward apoptosis might be regulated through changes in cellular CtBP levels. Previously, we have identified the homeodomain-interacting protein kinase 2 as such a regulator and demonstrated that HIPK2 activation causes Ser-422 phosphorylation and degradation of CtBP. In this study, we found that c-Jun NH2-terminal kinase 1 activation triggered CtBP phosphorylation on Ser-422 and subsequent degradation, inducing p53-independent apoptosis in human lung cancer cells. JNK1 has previously been linked to UV-directed apoptosis. Expression of MKK7-JNK1 or exposure to UV irradiation reduced cellular levels of CtBP via a proteasome-mediated pathway. This effect was prevented by JNK1 deficiency. In addition, sustained activation of the JNK1 pathway by cisplatin similarly triggered CtBP degradation. These findings provide a novel target for chemotherapy in cancers lacking p53

SIRT3 Protects Rotenone-induced Injury in SH-SY5Y Cells by Promoting Autophagy through the LKB1-AMPK-mTOR Pathway.

SIRT3 is a class III histone deacetylase that modulates energy metabolism, genomic stability and stress resistance. It has been implicated as a potential therapeutic target in a variety of neurodegenerative diseases, including Parkinson's disease (PD). Our previous study demonstrates that SIRT3 had a neuroprotective effect on a rotenone-induced PD cell model, however, the exact mechanism is unknown. In this study, we investigated the underlying mechanism. We established a SIRT3 stable overexpression cell line using lentivirus infection in SH-SY5Y cells. Then, a PD cell model was established using rotenone. Our data demonstrate that overexpression of SIRT3 increased the level of the autophagy markers LC3 II and Beclin 1. After addition of the autophagy inhibitor 3-MA, the protective effect of SIRT3 diminished: the cell viability decreased, while the apoptosis rate increased; α-synuclein accumulation enhanced; ROS production increased; antioxidants levels, including SOD and GSH, decreased; and MMP collapsed. These results reveal that SIRT3 has neuroprotective effects on a PD cell model by up-regulating autophagy. Furthermore, SIRT3 overexpression also promoted LKB1 phosphorylation, followed by activation of AMPK and decreased phosphorylation of mTOR. These results suggest that the LKB1-AMPK-mTOR pathway has a role in induction of autophagy. Together, our findings indicate a novel mechanism by which SIRT3 protects a rotenone-induced PD cell model through the regulation of autophagy, which, in part, is mediated by activation of the LKB1-AMPK-mTOR pathway