Biomedical subjects

Shasha Wu

Publications and source records attributed to Shasha Wu.

5 recordsLinked to original sources

PubMed2006

Spatiotemporal reasoning about epidemiological data.

OBJECTIVE: In this article, we propose new methods to visualize and reason about spatiotemporal epidemiological data. BACKGROUND: Efficient computerized reasoning about epidemics is important to public health and national security, but it is a difficult task because epidemiological data are usually spatiotemporal, recursive, and fast changing hence hard to handle in traditional relational databases and geographic information systems. METHODOLOGY: We describe the general methods of how to (1) store epidemiological data in constraint databases, (2) handle recursive epidemiological definitions, and (3) efficiently reason about epidemiological data based on recursive and non-recursive Structured Query Language (SQL) queries. RESULTS: We implement a particular epidemiological system called West Nile Virus Information System (WeNiVIS) that enables the visual tracking of and reasoning about the spread of the West Nile Virus (WNV) epidemic in Pennsylvania. In the system, users can do many interesting reasonings based on the spatiotemporal dataset and the recursively defined risk evaluation function through the SQL query interfaces. CONCLUSIONS: In this article, the WeNiVIS system is used to visualize and reason about the spread of West Nile Virus in Pennsylvania as a sample application. Beside this particular case, the general methodology used in the implementation of the system is also appropriate for many other applications. Our general solution for reasoning about epidemics and related spatiotemporal phenomena enables one to solve many problems similar to WNV without much modification.

Animals↗

PubMed2006

Transgenic mice that overexpress the anti-apoptotic Bcl-2 protein have improved histological outcome but unchanged behavioral outcome after traumatic brain injury.

Increasing evidence suggests that apoptosis is a contributing factor to neuronal cell death in traumatic brain injury (TBI). There is increased expression, cleavage and activation of caspases as well as other proteins known to regulate apoptosis in neurons after TBI. These proteins include the proto-oncogene Bcl-2 which belongs to a family of proteins with both pro- and anti-apoptotic properties. To investigate the role of apoptosis in TBI and the importance of Bcl-2 protein on the severity and outcome of injury, Bcl-2 overexpressing transgenic and wild-type control mice were subjected to the controlled cortical impact model of TBI. There was no significant difference in the cleavage of caspase-3 or caspase-9 detected by Western blotting of hippocampal samples from transgenic or wild-type mice after TBI. Bcl-2 transgenic mice had smaller contusion volumes and increased numbers of surviving neurons in CA2 but not other regions of hippocampus compared to wild-type controls. By contrast, there was no difference in motor function determined by the round beam balance and wire grip tests between transgenic and wild-type mice after TBI. Cognitive function assessed by the Morris water maze was also not different between groups. These results suggest that overexpression of Bcl-2 is only partially neuroprotective and other members of this protein family may prove to be more important in protecting neurons from cell death.

Animals↗

PubMed2004

c-FLIP-L recombinant adeno-associated virus vector infection prevents Fas-mediated but not nerve growth factor withdrawal-mediated cell death in PC12 cells.

Fas is a cell surface death receptor that may play an important role in regulating cell death in neuronal cell types by activation of caspase 8. Cellular FLICE inhibitory protein-long (c-FLIP-L) is an endogenous inhibitor of the activation of caspase 8 by Fas. The current study addresses the role of c-FLIP-L in regulation of cell death in PC12 cells induced by nerve growth factor (NGF) withdrawal and Fas antibody, which acts as a Fas ligand and activates the Fas receptor. A recombinant adeno-associated virus (rAAV) vector that expresses c-FLIP-L was constructed. PC12 cells infected with the c-FLIP-L rAAV were resistant to apoptosis induced by treatment with Fas antibody compared to cells infected with enhanced green fluorescent protein (EGFP) expressing rAAV. Overexpression of c-FLIP-L rAAV inhibited cleavage of caspase 8 induced by Fas antibody treatment. In contrast, treatment with the c-FLIP-L rAAV did not protect PC12 cells from cell death induced by NGF withdrawal. In conclusion, overexpression of c-FLIP-L rAAV inhibits Fas antibody-mediated cell death, but not NGF withdrawal-mediated cell death in PC12 cells.

Adenoviridae Infections↗

PubMed2000

[Using RevTet-On System to Control Thrombopoietin Gene Expression]

For the purpose of thrombocytopenia gene therapy, recombinant RevTet-On and pRevTRE/TPO retrovirus were packaged and transfected to NIH3T3 after selected with G418 and hygromycin, the two inserting recombinant retrovirus cell strain RevTet-On3T3/TPO were established. TPO expression was controlled and regulated by doxycydine (Dox). After using Dox to control the expression of TPO in RevTet-On3T3/TPO cells, the result showed that when Dox is added to the RevTet-On3T3/TPO cells, cell populations expressed TPO highly in the presence of 2 mg/L of Dox, and lowly in the absence of Dox. By using the RevTet-On gene expression system (the retrovirus vector RevTet-On regulation system to control the expression gene by Dox), it could modulate the expression of multiple genes by tetracyline and its derivatives. This system maybe provides a safe and efficacient way for the thrombocy to penia gene therapy.

Journal Article↗

PubMed2000

[p16 (CDKN2) Gene Transfer Mediated by Retrovirus Vector Inhibits Proliferation of Leukemia Cell Line K562]

The aim of this work was to test the effect of p16 on the proliferation of leukemic cells and its potential in gene therapy for leukemia. The full-length p16 cDNA was transfered by recombinant retrovirus vector into leukemia cell line K562, which is homozygous p16 deletion and retains functional retinoblastoma (RB) protein. The cell proliferation was tested in liquid and in soft agar culture after transduction of p16 retrovirus. The results showed a strong inhibition of cell proliferation. Phosphorylation of RB protein was also inhibited. The findings demonstrated that p16 (MTS/CDKN2) inactivation is a significant factor in the genesis and progression of leukemia and p16 could be a candidate gene for gene therapy in leukemia.

Journal Article↗