Objective To study the sequence of learning and memory loss in the rat after hemispheric irradiation. Methods After Sprague Dawly(SD) female rats were anaesthetized with chloral hydrate, their cerebral hemispheres were irradiated with a single dose of 5,15 or 30?Gy by 4?MeV electron. On D3,D7,D30 and D60, the learning and memorizing ability was measured with the Y maze test. Results On D3 and D7, the learning ability of SD rats was impaired most but partly restored in 1 to 2 months. In observation of memory loss, the intensity of cerebral function damage was in direct proportion to the increase of radiation dose.Conclusion The learning and memorizing ability of rats can be damage by hemispheric irradiation with the severity of impairment and possibility of recruitment depending on the dose.

The objective of study was to explore the role of vascular endothelial growth factor (VEGF) and its receptor-2 in pathogenesis of acute myeloid leukemia. The acute myeloid leukemia model was established on 20 mice with severe combined immunodeficiency (SCID) transplanted by HL-60 cells. The mice were divided into the normal control and test group randomly. The expression of VEGF was detected by enzyme linked immunosorbent assay (ELISA). The expression of VEGFR-2 mRNA was detected by RT-PCR. The results showed that the establishment of acute myeloid leukemia model was succeeded on all SCID mice by HL-60 cell transplantation. The expressions of VEGF and VEGFR-2 mRNAs could be determined on all mice. As compared with the normal control group, the expressions of VEGF and VEGFR-2 mRNAs in the test group significantly increased, but gradually increased during the course of disease. It is concluded that the abnormal expressions of VEGF and VEGFR-2 exist in mice with acute myeloid leukemia, which may be involved in the pathogenesis of AML.
Animals ; Bone Marrow ; pathology ; HL-60 Cells ; Humans ; Mice ; Mice, SCID ; Neoplasm Transplantation ; Vascular Endothelial Growth Factor A ; metabolism ; Vascular Endothelial Growth Factor Receptor-2 ; metabolism