OBJECTIVE:To discuss clinical pharmacists' role in clinical drug treatment. METHODS: Case study was performed retrospectively on clinical pharmacists' involving in clinical drug treatment. RESULTS & CONCLUSION: Hospital pharmacists' participating in drug treatment had achieved remarkable outcome. Clinical pharmacists have to cooperate with medical staff in clinical drug treatment so as to bring their due role into full play.

OBJECTIVE:To investigate the cognition of medical staff's cognition on clinical pharmaceutical care.METHODS:A total of 105 questionnaires collected from the doctors and nurses were subjected to an aggregate analysis in terms of their ultimate educational background,professional title,working lifetime,cognition on clinical pharmaceutical care etc.RESULTS & CONCLUSIONS:Doctors and nurses had positive attitude toward clinical pharmacy care and it is greatly demanded in drug use.Clinical pharmaceutical staff should keep improving their expertise level and strengthen cooperation with medical staff so as to facilitate the development of clinical pharmaceutical care.

Objective To observe the effect of autophagy on paclitaxel-induced CaSki cell death through the regulation of the expression of autophagy gene Beclin1, and to explore the interaction and relationship between autophagy and apoptosis. Methods Eukaryotic expression vector pcDNA3.1-Beclin1 and RNA interference vector pSUPER-Beclin1 were transfected into human cervical cancer CaSki cells in vitro and screened for stable expression cell lines. The formation of autophagic vacuoles was observed with an electronic microscope. The expression of Beclin1 and LC3 was measured by Western blot. After being treated with paclitaxel, the change of cell proliferation was assessed by MTT assay, the percentage of apoptotic cells and autophagic cells were analyzed by flow cytometry. Results A lot of autophagic vacuoles were observed in pcDNA3.1-Beclin1 cells by electronic microscopy. Beclin1 and LC3 protein expression was up-regulated in CaSki cells transfected with pcDNA3.1-Beclin1, and was inhibited in cells transfected with pSUPER-Beclin1. MTT assay revealed the survival rate of CaSki cells was significantly decreased after being transfected with pcDNA3.1-Beclin1. After being treated with paclitaxel, the percentages of apoptotic cells and autophagic cells were both increased in pcDNA3.1-Beclin1 group compared with that of the blank control group especially the increase of apoptosis was particularly evident. Conclusion Autophagy and apoptosis have different roles in the process of paclitaxel-induced cervical cancer CaSki cell line death. Overexpression of Beclin1 in CaSki cells may enhance the apoptosis induced by paclitaxel.

AIM: To study the effect and mechanism of Delicaflavone on migration and invasion of gefitinib-resistant lung cancer cell line PC-9/GR. METHODS: MTT assay was used to detect cell viability. Transwell and scratch assays were used to detect cell invasion and migration abilities. Western blotting was used to detect the expressions of MMP-9, MMP-2, E-cadherin, N-cadherin, Vimentin and PI3K/Akt/mTOR pathway-related proteins in PC-9/GR cells. RESULTS: Compared with control group, 20 mg/L Delicaflavone could significantly inhibit the viability of PC-9/GR cells for 24 h (P<0.05), while Delicaflavone below 10 mg/L had no significant effect on cell proliferation. The number of invasive cells and migrated cells were decreased significantly by Delicaflavone in a concentration-dependent way (P<0.05 and P<0.01). Delicaflavone could concentration-dependently reduce the expression of MMP-9, MMP-2, N-cadherin, vimentin (P<0.01), meanwhile up-regulate the expression of E-cadherin (P<0.01). In addition, Delicaflavone also decreased the expression of p-PI3K, p-Akt and p-mTOR in a concentration-dependent manner (P<0.01). CONCLUSION: Delicaflavone can inhibit the migration and invasion of PC-9/GR cells by regulating epithelial-mesenchymal transition via PI3K/Akt/mTOR pathway.