This article describes the progress of developing the training base and training methods for bronchoscopists at Changhai hospital in recent years,and then discusses the potential issues and solutions that might occure in the course of training,and finally explores the model and methodology to optimize the training program for Chinese bronchosocpists.

Objective To investigate the effects of ischemic preconditioning on pneumocyte apoptosis and the expression of HSFT0 after lung isehemia-reperfusion(I/R) in rats and discuss its possible mechanism of extenu-ating ischemia-repedusion injury. Method Thirtysix male Sprague-Dawley rats were randomly divided into three groups [ sham operation(SO ) group, ischemia-teperfusion(L/R) group, and ischemic preconditioning(IP) group],twelve in each group. Lung croas-clamping was used to build the L/R model. In IP group, three cycles of 5-minute-ischemia + 5-minute-reperfusion were given to the pulmonary artery before the procedure. Sham operation rats had a thoracotomy only. Two hours(or five hours) reperfusion was given to both L/R and IP group. Tenninal-deoxynucleotidyl Transferase Mediated d-UTP Nick End Labeiing(TUNEL) was used to evaluate apoptosis. Expression of HSP/0 in lung was observed by immunohistochemical stain and image analysis. Index of quantitative assessment of histologic lung injury(IQA), wet to dry weight ratio(W/D) were measured. The pathological change of lung tissue was observed under both hght and electron microscopy. Statistical analysis was carried out by One-way Anova. Scheffe test was used for intragroup comparison. Results The apoptosis index and expression of HSP70、W/D,IQA of hng tissue in I/R group were higher than those in the sham operation group (P<0.01). Compared with the L/R group, the apoptosis index and expression of HSP70, W/D, IQA of lung tissue significantly decreased (P<0.01), the levels of expression of HSPTO increased significantly in IP group ( P<0.01 ). The pathological and ultrastructure change of lung tissue was better in IP group than those in I/R group. Condusions Ischemic preconditioning can extenuate lung I/R injury by the possible mechanism of increasing the expression of HSPT0 which inhibits the apoptosis during lung I/R injury.

Objective： Our aim was to purity the modifier protein of glyceraldehyde-3-phosphate dehydrogenase　(G3PD)　from African green monkey Vero-E6 line. Methods：Exposure of Vero-E6 cells to medium with a reduced K concentration (3.2 mmol/L) stimulated the growth and activation of G3PD. The increase of enzyme activity was mediated by a cytosolic modifier protein that was purified using affinity and anion-exchange high-performance liquid chromatograph. Results：The apparent molecular mass of the protein was 62 kDa. Western blotting and quantiative enzyme-linked immunosorbent assay showed that the amount of modifier protein increased progressively for 2 hours in cells exposed to low-K+ medium, and then returned to the control value, a kinetic profile similar to that the modifier protein is a constituent of renal epithelial cells and accummulated transiently in the low-K+ mitogenic signal. Conclusion: We obtained a modifer protein from monkey kidney epithelial cells (Vero-E6). It could activate G3PD and cell growth.

Objective To investigate the effects of naloxone (Na) on pneumocyte apoptosis and expression of heme oxygenase-1 (HO-1) during ischemia reperfusion injury of lung in rats. Method Forty-two male Sprague-Dawley rats were made models of ischemia reperfusion injury of unilateral lung, and were randomly( random number) divided into three groups: sham operation group (Sh group), ischemia reperfusion group (IR group) and naloxone group (Na group). The hilus of lung was clamped for 45 minutes and the clamp was taken off to build the I/R model. After 3-6 hours reperfusion, naloxone in dose of 1 mg/kg was injected intra-peritoneally in rats of Na group. The rate of cell apoptosis in lung tissue was detected with the way of Annexin-V-PI in flow cy-tometer. The wet to dry weight ratio (W/D) of lung tissue was measured. The expression of HO-1 in lung was measured by using RT-PCR and the ultra-structure change of lung tissue was observed under electron microscope. Results The rate of pneumocyte apoptosis and W/D ratio of lung tissue were significantly higher in IR group than in Sh group (P < 0.01), and the rate of pneumocyte apoptosis and W/D ratio of lung tissue were negatively correlated with the expression of HO-1 mRNA in lung tissue. Compared with IR group, the rate of cell apoptosis and W/D ratio were lower and the expression of HO-1 mRNA was higher in Na group (P < 0.01). The ultra- structure changes of lung tissue were lessened in Na group than in IR group. Conclusions During early period of lung IR injury, HO-1 induced by naloxone can inhibit the cellular apoptosis and protect the lung tissue.

Tyrosinase is an important enzyme in controlling the formation of melanin in melanosome, and plays a key role in the pigmentation of hair and skin. The abnormal expression or activation of tyrosinase is associated with several diseases such as albinism, vitiligo, melanoma and Parkinson disease. Excessive deposition of melanin could cause diseases such as freckles and brown spots in the human body, and it is also closely related to browning of fruits and vegetables and insect molting. Detecting and inhibiting the activity of tyrosinase is of extraordinary value in the progress of diagnosis and treatment of these dis-eases. Therefore, many selective optical detection probes and small molecular inhibitors have been developed, and have made significant contributions to the basic and clinical research on these diseases. In this paper, the detection and inhibition of tyrosinase and their application in whitening products are reviewed, with special emphasis on development of fluorescent probes and inhibitors. Hopefully, this review will help design more efficient and sensitive tyrosinase probes and inhibitors, as well as shed light on novel treatment of diseases such as melanoma.