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Background & Objective: Recent studies have shown that wild-type p53 gene can enhance the chemosensitivity of the majority of non-small cell lung cancers. p73 gene and its homologue p53 gene have significant sequence and functional similarities. This study was designed to investigate the effect of p73 gene on chemosensitivity of human lung adenocarcinoma cells H1299., Methods: The pcDNA3-HA-p73alpha plasmid were transferred into in vitro cultured human lung adenocarcinoma cell line H1299 with Dosper. The p73alpha positive cells which were resistant to G418 were selected out. The expression of exogenous P73alpha protein were examined by Western blot analysis. MTT assay were used to analyze the response of transfected cells to cisplatin (cDDP),adriamycin (ADM). The drug-induced apoptosis of transfected cells was measured by flow cytometry and TUNEL technique. The biological behavior changes of the cells were observed by colony formation assay., Results: The transfected lung adenocarcinoma cell line H1299 overexpressed P73alpha protein stably. MTT assay showed that the IC(50) values for cDDP and ADM were reduced to approximate 86.2% and 99.2% in the transfected cells compared with the untransfected cells, respectively. The low concentration of chemotherapeutic drugs (1.25 micromol/L cDDP or 0.05 micromol/L ADM) without inhibition essentially suppressed the growth of the transfected cells markedly. The cDDP-induced apoptosis rate increased from 10.1% to 38.4%(P< 0.01). The ADM-induced apoptosis rate increased from 12.1% to 49.3%(P< 0.01). Colony-formation assays showed that the colony number in transfected cells was decreased significantly by chemotherapeutic drugs compared with parental cells(P< 0.01). The sensitive enhancement ratios for cDDP or ADM were 1.8 and 2.6, respectively., Conclusion: p73 gene was capable of enhancing the sensitivity of H1299 cells to chemotherapeutic drugs such as cDDP and ADM, and the increased sensitivity was associated with the induction of apoptosis undepend p53 gene. It suggests the possibility of using p73 gene combined with anticancer agents to improve the effectiveness of chemotherapy.

Objective: To study the effect of imbalance between lysosomal enzymes and their inhibitors in blood on disturbance of the local and whole body after trauma., Methods: The dynamic changes of lysosomal enzymes and proteinase inhibitors were studied in 12 pigs with femoral comminuted fractures in both hind limbs caused by high velocity missiles. Four normal pigs served as controls., Results: After injury, the activity of Cathepsin D in arterial plasma increased gradually and reached the highest level at 8 hours, acid phosphatase in serum began to increase at 12 hours and the value of serum elastase did not change significantly. The level of alpha1-antitrypsin, a proteinase inhibitor in plasma, decreased significantly in the early stage after injury [73.5%+/-6.4% and 81.0%+/-5.1% of the baseline value (1.67 micromol x ml(-1) x min(-1)+/- 0.29 micromol x ml(-1) x min(-1)) at l and 2 hours after injury, respectively, P<0.05], then increased gradually and was higher than the baseline value at 12 hours after injury., Conclusions: Imbalance between lysosomal enzymes and proteinase inhibitors occurs soon after injury, which might result in continuous tissue damage and play an important role in the disturbance of general reaction after injury.

Glucocorticoids (Gc) affect neuroendocrine function of hypothalamic-pituitary-adrenal axis (HPAA), especially of the hypothalamus. Synthesis and secretion of neuronal hormones of hypothalamus are associated with G-protein-linked signalling system. Here, the regulation by Gc of the levels of several G-protein alpha-subunits in rat hypothalamus was studied with Western blot method. Results showed that Gc downregulated Galphas1, Galphas2,Galphai and Galphaq with different magnitudes, being 14.37,15.66,14.61 and 12.37 per cent, respectively. However, Gc did not affect Galphao expression. Our results provided important information for understanding how Gc alters neuroendocrine function through G-protein-linked signalling system.