After the characteristics and necessity of medical informatics experimental course were analyzed, the application of three-stage case teaching in medical informatics experimental course was described, and its steps and methods were explained with the teaching contents of hospital system module used in experimental course as an example. This teaching method can strengthen the knowledge the students have learned.

Objective To study the possible pathogenesis of TNBS (2,4,6-trinitrobenzenesulfonic acid)-induced inflammatory bowel disease (IBD) in a mouse model by analyzing histological changes in colon and the expression of cytokines and transcription factor RORγt related to T cell subsets in mesenteric lymph nodes.Methods Female BALB/c mice aged 6-8 weeks were randomly grouped into two groups: IBD model and normal control groups.The mouse model of IBD was established by treating mice with 200 μl of 5％ TNBS/50％ ethanol solution (1∶1) through intestinal instillation, while the mice in the normal control group were instilled with PBS.Pathological changes in colon samples of mice were observed.Real-time PCR was performed to detect the dynamic expression of Th1 cytokines (IL-2, IFN-γ and IL-12p40), Th2 cytokine (IL-4), Treg-related cytokine (IL-10), Th17 cell-related cytokines (IL-17, IL-21 and IL-23) and transcription factor RORγt in mesenteric lymph nodes.Results The mice in the model group begun to show abnormal vital signs such as diarrhea, loss of weight and reduced activity, and mild hyperemia of intestinal mucosa and edema from the third day after modeling.Slight lesions were observed in histological slices of colon tissues stained with hematoxylin and eosin (HE).The expression of IL-21, IL-23 and IL-17 at mRNA level were significantly increased, while the expression of other cytokines showed no significant change.On the sixth day after modeling, many pathological symptoms and intestinal mucosal lesions were aggravated, and marked infiltration of inflammatory cells was observed in histological slices of colon tissues, which indicated that the IBD model was successfully induced by TNBS.Compared with the control group, the IBD model group showed significantly enhanced expression of IL-2, IL-12p40 and IL-10 in mesenteric lymph nodes at mRNA level on the sixth day after modeling.Although the expression of IL-21, IL-23, IL-17 and RORγt at mRNA level on the sixth day were down-regulated to different extent as compared with those on the third day, they were still significantly higher than those of the control group.Conclusion Th17 cell-related cytokines play an important role in the early stage of TNBS-induced IBD.With the progression of the disease, both Th1 and Th17 cells are involved in the immunopathological injury of colon tissues.

OBJECTIVE:To introduce a self-cure method for the cough caused by cold.METHODS:By placing control group and trial group,30 cases(control group)were assigned to receive Dextromethorphan Hydrobromide oral liquid and 32 cases(trial group)to employ self-cure method for cough caused by cold.And a self-cure method for the cough caused by cold was induced.RESULTS & CONCLUSION:The practice of self-cure method can speed up the self-cure of cough caused by cold and this method deserves to be popularized.

Objective To investigate the effects of remffentanil pretreatment on myocardial ischemiareperfusion (I/R) injury in rabbits. Methods Thirty healthy rabbits, aged 12-18 months, weighing 2.5-3.5 kg,were randomly divided into 3 groups (n = 10 each): I/R group, low-dose remifentanil pretreatment group (group R1 ) and high-dose remifentanil pretreatment group (group R2 ). Myocardial I/R was induced by ligation of anterior descending branch of left coronary artery for 30 min followed by 6 h of reperfusion in the 3 groups. Remifentanil was infused intavenously at 1.65 and 3.30 μg· kg - 1 · min- 1 for 30 min before ischemia in group R1 and R2 respectively, while equal volume of normal saline was infused instead in group I/R. Blood samples were taken for determination of serum cardiac troponin-Ⅰ (cTnI) and creatine kinase-MB isoenzyme (CK-MB) concentrations before administration (baseline), after administration, at 30 min of ischemia and at 6 h of reperfusion. The rabbits were then sacrificed and hearts removed. Myocardial tissues were obtained for microscopic examination. Results Serum cTnI and CK-MB concentrations were significantly lower in group R1 and R2 than in group I/R and serum cTnI concentration lower in group R2 than in group R1 ( P ＜ 0.01). Remifentanil infusion significantly attenuated the pathologic changes in a dose-dependent manner. Conclusion Remifentanil pretreatment provides protective effect against myocardial I/R injury in rabbits and it is related to the dose.

BACKGROUND:Hyperbaric oxygen(HBO)treatment promotes the proliferation and differentiation of endogenous neural stem cells in neonatal rats following hypoxic/ischemic brain damage(HIBD).The Wnt signaling pathway is associated with neurogenesis.However,there are few data recording the role of HBO in the differentiation of neural stem cells in vitro.OBJECTIVE:To observe the effect of HBO on differentiation and Wnt3 expression of bone marrow mesenchymal stem cells(BMSCs).METHODS:BMSCs were isoiated and cultured.The rat BMSCs of passages 3-5 were cultured in DMEM/F12(1:1)medium with basic fibroblast growth factor,epidermal growth factor and B27 for 24 hours.The induced BMSCs were randomly divided into two groups:control group(no treatment)and HBO group(HBO,0.10 MPa,60 minutes stabilizing pressure with at least 90% oxygen).The neuron specific encloase(NSE),glial fibrillary acidic protein(GFAP)and 04 marked oligodendrocyte immunocytochemistry were detected by immunofluorescent staining,and Wnt3 protein expression was detected by Western-blot.RESULTS AND CONCLUSION:BMSCs cultured in classic medium of neural stem cells could significantly induce the expression of nestin.The expression of NSE and 04 of HBO group was greater than control group(P＜0.01),but GFAP expression displayed no significant difference between the groups(P＞0.05).Western blot showed HBO could enhance the Writ3 expression (P＜0.05).Results show that HBO can induce BMSCs to differentiate into neural cells and oligodendrocyte,which is correlated with the activation of the Wnt3 protein.

AIM: To explore the influence of different concentration midazolam on the macroscopic voltage gated potassium currents and to discuss the relationship between potassium currents and inhibitory effect of clinical relevant concentration midazolam on sympathetic nervous system. METHODS: Superior sympathetic ganglion neurons were dissociated enzymatically from 7 to10 day old rat. Experiments were performed about 5 h after plating at room temperature (20- 24 ℃ ). Appropriate solution was chosen to separate the K + current from the other transmembrane currents. 1 ?mol?L -1 TTX was applied to the extracelluar solution to block the Na + current. Midazolam was also resolved in extracelluar solution to get various concentration ( 0.1 , 0.3 ,3,10,50,100 ?mol?L -1 ). Currents were recorded with the patch clamp technique in whole cell configuration using glass electrodes with a tip resistance of 2- 4 M . Potassium currents were evoked by test pulse from -100 mV to +30 mV with holding potential -80mV. Data were analyzed using Clampfit 6.0 and Oringih 5.0 software. Whole cell current records were corrected for leakage and capacitance by using the P/5 protocol. RESULTS: Midazolam dose dependently inhibited the whole cell potassium currents. Clinical relevant concentration midazolam ( 0.3 ?mol?L -1 ) only reduced the peak currents by 3.89 %(P= 0.88 ). The concentration required to produce 50% current inhibition(IC 50 ) was 76.065 ?mol?L -1 . CONCLUSION: Midazolam inhibits the whole cell potassium current significantly and dose dependently, but clinical relevant concentration midazolam has minor effect on the potassium currents, indicating that the inhibitory effect of midazolam on potassium current is not related to the suppression of activity of sympathetic system.

OBJECTIVE:To investigate the improvement of the optimization of Hospital information system(HIS)for the hos-pital pharmacy. METHODS:Based on management practive of the hospital and relative national requirements,the improvement and optimization of HIS function was achieved by pharmacists and software engineers. The effects of its optimization on pharmaceu-tical care were also introduced,involving hospital drug supply,pharmaceutical administration and monitoring of rational drug use. RESULTS & CONCLUSIONS:HIS has new functions,such as web query of secondary drug inventory,electronic management of narcotic and psychotropic drugs,electronic prescription comments,color code for TCM incompatibility management,antibiotics re-porting,etc. Compared with previous system,optimized system is more perfect in terms of full inventory tracking,web query of the drug batch number,web query of supply information,electronic management of purchasing invoice,prescription comments and monitoring of rational drug use. It decreases workload of pharmacist greatly,and increases work efficiency and accuracy. Continu-ous optimization of HIS can improve pharmaceutical care,and play an importance role on the safety,rationality and effectiveness of drug use in patients.

Objective:To observe the effect of different concentration HMGB1 on the secretion of TNF-αand NO from Ana-1 infected with DEN2 and virus copy.Methods:DEN2 were proliferated and identified by conventional methods.The adherence of DEN2 to Ana-1 was observed by direct immunofluorescence and RT-PCR.The level of virus mRNA were detected by qRT-PCR.The concentration of TNF-αwas detected by ELISA.The concentration of NO was detected with Griess reagent.Results:Ana-1 was able to adhered for DEN2.Compared with DEN group,the inhibition ratio(%) of the level of virus mRNA in D-HMGB1-1 group,D-HMGB1-10 group,D-HMGB1-100 group,D-HMGB1-1000 group was 41.53 ±2.12,55.30 ±1.59,74.75 ±1.12,86.35 ±1.42.Compared with DEN group,the level of TNF-αand NO decreased in D-HMGB1 groups(P<0.05).Conclusion:HMGB1 can be effectively regulated of Ana-1 secreted inflammation factor of infected with DEN2,and inhibited DEN2 replication.

Objective To study the effect of recombinant human endostatin (rhES)on the radiosensitivity of esophageal squamous cells KYSE-150 and its preliminary mechanism.Methods Cells were divided into four groups:control group without treatment,rhES group treated with recombinant human endostatin,radiation alone group exposed with X-rays,and combination group exposed with X-rays plus endostatin.Colony formation assay was used to measure cell survival fraction.A single-hit multi-target model was used to fit cell survival curve and calculate the sensitive enhancement ratio (SER).Influence of rhES combined with X-ray radiation on cell cycle and apoptosis was measured by flow cytometry.Expressions of Cyclin B1,Cyclin D1,Bcl-2 and Bax mRNAs were determined by RT-PCR.Protein expressions of HIF-1α,VEGF,and VEGFR were determined by Western blot.Results D0,Dq and SF2 value of KYSE-150 cells decreased along with the concentration of rhES.At D0dose,the SER for 100 and 200 μg/ml rhES was 1.14 and 1.27,respectively.Compared with the radiation alone group,the apoptosis rate and bax expression increased,while the expressions of VEGF and HIF-1α decreased in the combination group (t =7.97,3.02,117.55,7.22,P ＜ 0.05).Conclusions rhES has radiosensitive effect on esophageal carcinoma cells KYSE-150 in vitro by inhibiting the expressions of HIF-1α and VEGF,regulating bax expression,and inducing apoptosis.

Objective To investigate the effects of interleukin-17 (IL-17) on the cell proliferation, apoptosis and migration of human laryngeal carcinoma Hep-2 cells.Methods IL-17 was transiently transfected into Hep-2 cells, and at the same time empty vector group (pEGFP-N1) and normal control group were set up.The efficiency of transfection was evaluated by fluorescence microscope, and the mRNA and protein expressions of IL-17 were detected by reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting.The proliferation of cells was detected by methyl thiazolyl tetrazolium (MTT) method, and the apoptosis was detected by flow cytometry.The migration ability was detected by wound-healing assay and Transwell assay.ResultsHep-2 cells transfected with empty vector pEGFP-N1 and IL-17 showed green fluorescence under the fluorescence microscope.Hep-2 cells expressed IL-17 at both mRNA and protein levels after transfection with IL-17.Compared with the normal control group, the proliferation of IL-17 transfected Hep-2 cells was significantly inhibited after 48 h transfection (0.34±0.03 vs.0.46±0.04, P=0.006).The apoptotic rate of IL-17 transfected cells was higher than that of normal control group (26.80%±0.80% vs.2.90%±0.31%, P=0.000).According to the wound-healing assay, compared with the normal control group, the scratch width of IL-17 transfected cells was significantly greater (1.59±0.01 vs.1.36±0.01, P=0.000).Transwell migration experiment showed that the migration of IL-17 transfected cells was significantly lower than that of the normal control group (26.33±2.08 vs.49.33±1.53, P=0.000).Conclusion IL-17 can inhibit the proliferation of human laryngeal carcinoma Hep-2 cells, reduce their migration ability and enhance their apoptosis ability.Therefore, IL-17 may inhibit the occurrence and development of laryngeal carcinoma through a variety of mechanisms.