Effects of granulocyte colony-stimulating factor on repair of injured canine arteries / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Endothelial progenitor cells (EPCs) derived from bone marrow may differentiate into endothelial cells and participate in endothelial repair. These cells can be mobilized into peripheral blood by cytokines, including granulocyte colony-stimulating factor (G-CSF). In the present study, we investigated the effects of G-CSF on neointimal formation and restenosis in a canine model of arterial balloon injury.</p><p><b>METHODS</b>Sixteen male beagle dogs were injected subcutaneously with 20 microg x kg(-1) x d(-1) recombinant human G-CSF (n = 8) or normal saline (n = 8) for 1 week. On the fifth day of treatment, the dogs underwent renal arterial angioplasty. At 8 weeks after arterial balloon injury, angiographic observations were made and injured arteries were processed for morphometric analysis of neointimal formation.</p><p><b>RESULTS</b>Peripheral white blood cell counts were increased by 3.34-fold compared to baseline on the fifth day of administration of G-CSF. Angiographies revealed that one stenosis had occurred among the eight injured renal arteries from dogs treated with G-CSF, whereas all injured renal arteries from dogs treated with normal saline remained patent. The mean extent of stenosis among injured arteries was 18.3% +/- 17.9% in the G-CSF treated group compared to 12.5% +/- 7.6% in the saline treated control group (P = 0.10). G-CSF treatment slightly increased neointimal thickness (0.42 +/- 0.15 mm vs 0.25 +/- 0.06 mm, P = 0.08) with an intima to media ratio of 0.83 +/- 0.49 vs 0.54 +/- 0.18 (P = 0.11).</p><p><b>CONCLUSIONS</b>G-CSF treatment does not attenuate neointimal hyperplasia and restenosis formation in a canine model of renal arterial injury, suggesting that the therapeutic strategy for preventing restenosis by stem cell mobilization should be investigated further.</p>

Relationship of HepG2 cell sensitivity to continuous low dose-rate irradiation with ataxia-telangiectasia mutated phosphorylation / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the changes of ataxia-telangiectasia mutated (ATM) phosphorylation in HepG(2) cells in relation to HepG(2) cell survival under continuous low dose-rate irradiation.</p><p><b>METHODS</b>HepG(2) cells were exposed to equivalent irradiation doses delivered at either a continuous low dose-rate (7.76 cGy/h) or a high dose-rate (4500 cGy/h), and the phosphorylated ATM proteins and surviving fraction of HepG(2) cells after the exposures were compared.</p><p><b>RESULTS</b>The phosphorylation of ATM protein was maximal at 0.5 Gy irradiation delivered at either a high doserate or a continuous low doserate. As the radiation dose increased, ATM protein phosphorylation decreased under continuous low dose-rate irradiation, but remained stable under high dose-rate irradiation. With comparable ATM protein phosphorylation induced by continuous low dose-rate irradiation and high dose-rate irradiation, there was no significant difference in the surviving fraction of HepG(2) cells (P>0.05), but at a significantly lower ATM protein phosphorylation level than that induced by high dose-rate irradiation, continuous low dose-rate irradiation resulted in increased cell killing (P<0.01).</p><p><b>CONCLUSION</b>Continuous low dose-rate irradiation increases HepG(2) cells radiosensitivity as compared with high dose-rate irradiation. Increased cell killing following continuous low dose-rate irradiation is associated with reduced phosphorylated ATM protein, and inhibition of ATM phosphorylation may increase the radiosensitivity of HepG(2) cells.</p>

Safety evaluation of iodine-125 seed implantation in rabbit liver tissue / 南方医科大学学报

<p><b>OBJECTIVE</b>To evaluate the safety of iodine-125 seed implantation in the liver.</p><p><b>METHODS</b>Twenty New Zealand rabbits were divided into control and treatment groups and in the latter, iodine-125 seeds of 37 MBq were implanted into the liver under CT guidance whereas nonradioactive seeds were implanted in the control rabbits. Four weeks after implantation, white blood cell count, liver functions, and renal functions were measured or evaluated for comparison with those before implantation. The rabbits were then anesthetized to collect the liver tissue for pathological examination with HE staining and cell apoptosis assay.</p><p><b>RESULTS</b>Obvious hepatic tissue necrosis was observed around the radioactive seeds in the treatment group. At a 5 mm distance to the seeds, a distinct boundary occurred between the necrotic hepatic cells and normal cells. The control rabbits, however, had normal liver structure around the seeds implanted. In situ cell apoptosis examination showed a distinct band of apoptotic cells in the liver tissue of rabbits in the treatment group, which was not found in the control group. Two weeks after iodine-125 irradiation, alanine aminotransferase significantly increased in the treatment group (t=6.285, P<0.001), but recovered two weeks later (t=2.002, P=0.06). No significant alterations occurred in aspartate aminotransferase, blood urea nitrogen, serum creatinine, hemoglobin, serum total bilirubin, white blood cell count, or platelet count after the seed implantation.</p><p><b>CONCLUSION</b>Iodine-125 seed implantation in the liver results in conformal irradiation dose distribution without obvious effects on the vital organs, demonstrating iodine-125 seed implantation as a safe and minimally invasive technique for hepatic cancer treatment.</p>