OBJECTIVE:To provide reference for improving teaching quality for pharmaceutical engineering major of Pharma-cology Course. METHODS:According to the current status and deficiencies on Pharmacology Course in universities,combined with own teaching experience and understanding,the author explored,four aspects. RESULTS & CONCLUSIONS:Pharmaceutical engineering major lacks specialized text books,and is in short of class periods and absence of experimant classes. Establishing rea-sonable teaching evaluation feedback mechanism,innovating teaching mode,setting up virtual simulation laboratory and sharing network resource may stimulate the enthusiasm of the students’self-learning,cultivate the students' ability to apply knowledge to practice and contribute to the improvement of teaching quality.

Objective:To study the influencing factors in the preparation of salicylic acid dropping pills , and determine the opti-mum preparation process .Methods: The environmental factors , heating temperature , matrix ratio and preparation steps of salicylic acid drop pills were observed .With pill weight difference , dissolution time and appearance quality as the indices , an orthogonal test was adopted to optimize the preparation process .Results:Salicylic acid and the matrix should be separately heated to prevent red ox-ide.The optimized preparation process of drop pills was as follows:the ratio of PEG 400 and PEG 6000 was 1∶5, the temperature of drug solution was 50℃, the dropping distance was 8 cm and the dropping rate was 70 drops per minute .Conclusion:The preparation process is simple and practicable .The pill weight difference , dissolution time and appearance quality all meet the quality require-ments.

C-reactive protein (CRP), an acute-phase protein with an ability to bind to nuclear antigen, has been reported to regulate cytokine secretion and modulate immune responses. We previously reported that activated syngeneic lymphocyte-derived apoptotic DNA (apopDNA) could induce macrophage activation and contribute to the initiation and progression of lupus nephritis. It is reasonable to hypothesize that CRP might regulate apopDNA-induced macrophage activation. Herein, CRP was shown to promote macrophage-mediated apopDNA uptake by binding to apopDNA (CRP/apopDNA complex). Notably, CRP/apopDNA treatment inhibited the production of inflammatory cytokines and chemokines by macrophages which could be induced by apopDNA alone. Further coculture and transwell studies revealed that CRP/apopDNA-induced macrophages prohibited apopDNA-induced macrophage activation in an IL-10 dependent manner. These results provide insight into the potential mechanism of CRP regulatory activity in macrophage activation induced by apopDNA in the context of lupus nephritis and other autoimmune diseases.
Animals ; C-Reactive Protein ; metabolism ; pharmacology ; Cell Line, Tumor ; DNA ; metabolism ; pharmacology ; Enzyme-Linked Immunosorbent Assay ; Female ; Lupus Erythematosus, Systemic ; metabolism ; Lupus Nephritis ; metabolism ; Macrophage Activation ; drug effects ; physiology ; Mice ; Mice, Inbred BALB C ; Protein Binding ; Real-Time Polymerase Chain Reaction

The bromodomain and extraterminal (BET) family member BRD4 is pivotal in the pathogenesis of cardiac hypertrophy. BRD4 induces hypertrophic gene expression by binding to the acetylated chromatin, facilitating the phosphorylation of RNA polymerases II (Pol II) and leading to transcription elongation. The present study identified a novel post-translational modification of BRD4: poly(ADP-ribosyl)ation (PARylation), that was mediated by poly(ADP-ribose)polymerase-1 (PARP1) in cardiac hypertrophy. BRD4 silencing or BET inhibitors JQ1 and MS417 prevented cardiac hypertrophic responses induced by isoproterenol (ISO), whereas overexpression of BRD4 promoted cardiac hypertrophy, confirming the critical role of BRD4 in pathological cardiac hypertrophy. PARP1 was activated in ISO-induced cardiac hypertrophy and facilitated the development of cardiac hypertrophy. BRD4 was involved in the prohypertrophic effect of PARP1, as implied by the observations that BRD4 inhibition or silencing reversed PARP1-induced hypertrophic responses, and that BRD4 overexpression suppressed the anti-hypertrophic effect of PARP1 inhibitors. Interactions of BRD4 and PARP1 were observed by co-immunoprecipitation and immunofluorescence. PARylation of BRD4 induced by PARP1 was investigated by PARylation assays. In response to hypertrophic stimuli like ISO, PARylation level of BRD4 was elevated, along with enhanced interactions between BRD4 and PARP1. By investigating the PARylation of truncation mutants of BRD4, the C-terminal domain (CTD) was identified as the PARylation modification sites of BRD4. PARylation of BRD4 facilitated its binding to the transcription start sites (TSS) of hypertrophic genes, resulting in enhanced phosphorylation of RNA Pol II and transcription activation of hypertrophic genes. The present findings suggest that strategies targeting inhibition of PARP1-BRD4 might have therapeutic potential for pathological cardiac hypertrophy.