OBJECTIVE:To improve the teaching quality of pharmaceutical standard training. METHODS: By introducing the overview of adopting elicitation teaching in the pharmaceutical standard training in Beijing,the training effect was summarized and role and significance were studied. RESULTS:Supervisors applied five teaching modules in the elicitation teaching in the pharmaceu-tical standard training which are concluded“pharmaceutical education and rational use of medicine”“comments of prescription and rational use of medicine”“prescription transfers and rational use of medicine”“medicine counseling and rational use of medicine”“pharmaceutically communication and rational use of drugs medicine”,the result showed that participants had mastered more than 90%of what they had learned;with 92.5%of participants felt elicitation teaching could help improve students’interests in pharma-cy,and strengthen responsibility;80.0% of the participants believed that part of the modules strengthen the training of clinical think-ing;the training of satisfaction to 100%. CONCLUSIONS: The elicitation teaching mode can not only improve the teaching quality in pharmaceutical standard training,but also strengthen communication and feedback between teachers and students,students and students to make students more deeply understand and master knowledge and improve teaching quality.

Objective:To study the possible immune escape mechanisms of HCoV-OC43 from human dendritic cells(DC).Methods:HCoV-OC43 was isolated from clinical specimen using BSC-1 cells and identified by Real-time PCR,and the cytopathic effect was observed by phase contrast microscope.DCs were induced in vivo using hu-GM-CSF and IL-4 cytokines,and after 7 days of differentiation,DCs were infected by HCoV-OC43.The morphology of HCoV-OC43 infected DC was observed by transmission electron microscope,and the cytokines related to DC functions were detected by Real-time PCR after infection.DC proportion and function related co-stimulatory molecules were analyzed by flow cytometry.Results:In vitro HCoV-OC43 infected human DC model was successfully built.HCoV-OC43 can infect DC and generate immune response of DC in vitro,but no virus nucleonic acid could be detected in culture supernatant.The DC expression of IFN-α,IFN-β,CCL3 and CCL5 were significant decreased when infected with HCoV-OC43,but the expression of costimulatory molecules including HLA-DR,CD1c and CD86 were not affected by HCoV-OC43 infection.Conclusion:Human DC could be infected by HCoV-OC43 and generate immune response,but could not produce progeny virus.HCoV-OC43 may escape from immune response by suppressing the expression of IFN-α and other inflammatory cytokines and chemokines in DC.

Objective To investigate characteristics of bleeding caused by combination of aspirin with ticagrelor in the treatment of Ischemic stroke (IS) and Transient Ischemic Attack (TIA),and analyze the risk factors influencing the occurrence of bleeding. Methods 501 patients with IS and TIA who were treated with aspirin combined with ticagrelor were included. And baseline and clinical data of the subjects were collected on the first day after admission,and the occurrence of bleeding events within one year was followed up. Patients were divided into two groups according to whether there was bleeding. Baseline and clinical data of the two groups were compared,and risk factors of bleeding events were analyzed by logistic regression. Results After 1 year of follow-up,a total of 89 patients were found to have bleeding,with a total bleeding rate of 17.76%,a fatal bleeding rate of 5.39% and a non-fatal bleeding rate of 12.38%. In 5.19% of patients,ticagrelor was discontinued due to bleeding,while in 7.58% of patients,the dosage of ticagrelor was halved due to bleeding. Logistic regression analysis found that age,smoking history,history of myocardial infarction,history of peptic ulcer and CRUSADE score≥41 are risk factors for bleeding events (P<0.05). Conclusion 17.76% of IS and TIA had bleeding events during aspirin combined with ticagrelor,and age,smoking history,history of myocardial infarction,history of peptic ulcer disease,and higher CRUSADE score were risk factors for bleeding.

Objective: To investigate the molecular evolution characteristics of human coronavirus (HCoV) subtypes in patients with fever and respiratory tract infection in Guangzhou from 2010 to 2012. Methods: Partial fragments of NP, RdRp and S genes of HCoV-OC43, HCoV-229E and HCoV-NL63 positive samples were amplified by RT-PCR and sequencing. Bioinformatics software, including Bio-edit, Mega4.0 and Clustal1.83 were used for comparison and analysis of NP, RDRp and S gene sequences. Molecular evolutionary tree of different gene regions of HCoV-OC43, HCoV-229E and HCoV-NL63 were built. Results: No remarkable variation or recombinant strain of HCoV-OC43, HCoV-229E and HCoV-NL63 was found in Guangzhou during 2010—2012. The HCoV-OC43 substrains were genetically closest to the strains found in Belgium and Hong Kong (GenBank accession number JN129834 and AY903460). HCoV-229E substrains were genetically closest to those found in Amsterdam (GenBank accession number JX503060) and HCoV-NL63 most genetically close to those in Amsterdam and Beijing (GenBank accession number JX104161 and DQ445911). The NP and RDRp genes of all subtypes were highly conserved, while S gene was more variable. Conclusions There were at least 3 substrains of HCoV-OC43, HCoV-229E and HCoV-NL63 epidemic in Guangzhou during 2010—2012, and no remarkable variation or recombinant viral strain was found. The NP and RDRp genes of all subtypes were highly conserved and can be used in virus detection, while S gene was more variable and suitable for phylogenetic and variation study.

Currently, there is still no effective curative treatment for the development of late-stage liver fibrosis. Here, we have illustrated that TB001, a dual glucagon-like peptide-1 receptor/glucagon receptor (GLP-1R/GCGR) agonist with higher affinity towards GCGR, could retard the progression of liver fibrosis in various rodent models, with remarkable potency, selectivity, extended half-life and low toxicity. Four types of liver fibrosis animal models which were induced by CCl₄, α-naphthyl-isothiocyanate (ANIT), bile duct ligation (BDL) and Schistosoma japonicum were used in our study. We found that TB001 treatment dose-dependently significantly attenuated liver injury and collagen accumulation in these animal models. In addition to decreased levels of extracellular matrix (ECM) accumulation during hepatic injury, activation of hepatic stellate cells was also inhibited via suppression of TGF-β expression as well as downstream Smad signaling pathways particularly in CCl₄-and S. japonicum-induced liver fibrosis. Moreover, TB001 attenuated liver fibrosis through blocking downstream activation of pro-inflammatory nuclear factor kappa B/NF-kappa-B inhibitor alpha (NFκB/IKBα) pathways as well as c-Jun N-terminal kinase (JNK)-dependent induction of hepatocyte apoptosis. Furthermore, GLP-1R and/or GCGR knock-down results represented GCGR played an important role in ameliorating CCl₄-induced hepatic fibrosis. Therefore, TB001 can be used as a promising therapeutic candidate for the treatment of multiple causes of hepatic fibrosis demonstrated by our extensive pre-clinical evaluation of TB001.