To meet the need of cultivating high-quality personnnel,enhance the medicalstudents' ability to analyze and solve problems,directing at the problems existed in pharmacology experiment,we have adjusted and reformed the content of the experiment teaching in pharmacology and conducted the survey and research among the students so as to lay a solid fundation to its reasonable implement.

Objective:To investigate the role of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) in regulating proliferation of airway smooth muscle cells in ovalbumin(OVA)-induced asthma rats. Methods：Male Wistar rats (n=16) were randomized into OVA-induced asthma group and control group(8 rats each). The histomorphological changes of bronchia and lung tissues were observed by H-E staining. The expressions of proliferating cell nuclear antigen(PCNA) and PTEN were assayed by immunohistochemistry. Reverse transcription-polymerase chain reaction(RT-PCR) was carried out to determine the changes in the expression of PTEN mRNA. Results: The typical pathological features of asthma were revealed in the OVA-exposed rats including numerous inflammatory cells infiltrated around the bronchia and in the lung tissues, the thickened airway smooth muscle and the narrowed airway. The levels of PCNA were distinctly increased in OVA-induced asthma group than that of control（P < 0.05），while the levels of PTEN and PTEN mRNA were significantly decreased in lung tissues of OVA-exposed rats（P < 0.05）. Conclusion：The gene inactivation of PTEN may play a pivotal role in proliferation of airway smooth muscle cells in asthma rats, and the most probable mechanism is associated with the functions of PI3K signaling pathway.

In this study, hollow fiber membrane extraction combined with ambient ionization mass spectrometry ( AMS) was developed for the simultaneous determination of 7 perfluorinated compounds ( PFCs) in aqueous solution, including perfluoroheptanoic acid ( PFHpA ) , perfluorooctanoic acid ( PFOA ) , perfluorooctane sulfonate acid ( PFOS ) , perfluorononanoic acid ( PFNA ) , perfluorodecanoic acid ( PFDA ) , perfluoroundecanoic acid ( PFUdA) , and perfluorododecanoic acid ( PFDoA) . PFCs were detected in negative ion mode using selective reaction monitoring ( SRM) mode. The extraction time and the pH value of extraction solution were optimized. 13 C4-PFOS and 13 C4-PFOA were used as internal standards for quantitative analysis. The method showed good linearity with correlation coefficient values ( r2 ) greater than 0. 991 for the seven target PFCs. With the exception of PFHpA, the limit of detection ( LOD) for other six PFCs was within ranges from 0. 8 to 2. 7 ng/L while the limit of quantitative (LOQ) was from 2. 7 ng/L to 8. 9 ng/L. The enrichment factor of five PFCs was more than two hundred. The developed method was applied to detect the seven PFCs in tap water and Pearl River water, and they were all not detected. The recoveries were within the ranges of 88. 5%-108. 3% and 94. 2%-116. 7% when 40 ng/L and 400 ng/L PFCs were spiked into tap water, respectively. In terms of the Pearl River water, the recoveries were within the ranges of 75. 0%-102. 6% and 81. 2%-97. 6% when 40 ng/L and 400 ng/L PFCs were spiked, respectively.

This study is to investigate protective effect of safflor yellow B (SYB) against vascular endothelial cells (VECs) injury induced by angiotensin-II (Ang-II). VECs were cultured and divided into six groups: control group, Ang-II group, Ang-II + SYB (1 micromolL(-1)) group, Ang-II + SYB (10 micromolL(-1)) group, Ang-II + SYB (100 micromolL(-1)) group and Ang- II + verapamil (10 micromolL(-1)) group. Except control group, all of VECs in other groups were treated with Ang- II at the final concentration of 0.1 micromolL(-1). Mitochondria membrane potential (MMP) and free calcium concentration ([Ca2+]i) were measured by laser scanning confocal microscopy, and mitochondria complex IV activity was detected by BCA method. The levels of reactive oxygen species (ROS) in VECs were analyzed by fluorescence detector and apoptosis of VECs was observed by flow cytometer. Caspase 3 was determined by Western blotting method. Comparing with control group, Ang-II was able to increase [Ca2+]i and ROS level, decrease MMP level, inhibit complex IV activity and enhance caspase 3 activity in VECs, as a result, enhance apoptosis of VECs. But SYB could significantly reduce the result induced by Ang- II relying on different dosages (P < 0.05 or P < 0.01). SYB was able to eliminate the effect of Ang-II on VECs via regulating [Ca2+]i, mitochondrial structure and function and inhibiting apoptosis.

Objective To study the signal transduction pathway genes in acute respiratory distress syndrome(ARDS) of rats by gene chip. Methods Total RNAs were isolated from lungs of normal and ARDS rats respectively. The RNAs were purified by oligotex. Both mRNAs from two kinds of tissues were reversely transcribed to cDNA with incorporation of fluorescent-labelled dUTP to prepare the hybridization probes. The mixed probes were hybridized to cDNA microarray. Picture signals of fluorescence in gene array were scanned and compared by CapitlBio Molecule Annotation System V4.0. Quantitative fluorescence RT-PCR was used to validate the results of genechip. Results The results showed that there were 2 genes up-regulated and 9 genes down-regulated in lung tissue of ARDS rats,and these genes were involved in 11 signal transduction pathways. Conclusion Many genes of signal transduction pathways expressed in ARDS transcription profiles of rats.