The basic nature of medical ethics education is the cultivation of morality for medical students,in which humanistic spirit is the fundamental element.Humanistic spirit is in great need for the development of medical ethics,the transformation of medical mode,the harmonious development of physician-patient relationship,and the healthy growth of medical students.Based on present realistic conditions,humanistic spirit should be developed in the fields of classroom training,medical professional education,and other aspects of campus culture.It would be necessary to find multi-path training modes of humanistic spirit.

The specialization of medical science determines the objective existence of asymmetric information in medical and health industry.These different understandings in the psychological and behavioral area influenced the development of physician-patient relationship.Medical personnel should look squarely at the professional attributes and dare to play a leading role.Meanwhile,the exchange of the role of patient and medical personnel,understanding patient,clearing of communication channels and enlarging patients′ means of communication will promote harmonious relations between doctors and patients.

Objective To explore the signal transduction mechanism of inhibitor kappa B kinase α( IKKα) , one of the catalytic subunits of IKK complex , for regulating p53 transactivation in the cellular ultraviolet radiation ( UVB) repsonse. Methods The transactivation of p53 was determined by dual-luciferase reporter gene analysis system while the expression and activation of IKKα, IKKβ, p53 and p38K was detected by Western blotting assay .Results UVB exposure induced activation and transactivation of p 53 in the wild type mouse fibroblasts ,but the effect was blocked by IKKa deficiency and recovered by reconstitution of IKKαexpression.Under the same conditions , IKKαregulated p38K activation, while inhibi-ting p38K activation down-regulated p53 transactivation under UVB exposure .Conclusion IKKαregulates UVB-induced phosphorylation and activation of p 53 in a p38K-dependent manner .

Objective To systematically study solvatomorphism of indomethacin and provide a scientific basis for the quality control of the solvated impurities in this drug. Methods By changing the recrystallization solvent, solvent volume, recrystallization temperature, time and pressure, nine solvates and four non-solvated forms were discovered and prepared. The differential scanning calorimetry (DSC), thermogravimetric analysis ( TGA), X-ray powder diffraction ( PXRD) and infrared spectrometry (IR) were introduced for characterization analysis. Furthermore, the test of influencing factors was used to explore the stability of solvate crystal form and the crystal transformation rules among them. Results Nine solvates were prepared, which including two solvates reported for the first time in this work. Results showed that crystal forms of the 9 solvates have different types or proportions of crystal solvents according to the various results of DSC, TGA, PXRD and IR. Moreover, the nine solvates prepared in this work were metastable crystal forms which could be transformed to non-medicinal forms. Conclusion The composition, thermodynamic property and transformation rule of all the solvates are elucidated in this work. In addition, an effective method for qualitative or quantitative analysis of these solvates was established. The standard graphs and data were used as basic data and scientific basis for the solvate control in the manufacturing of indomethacin.

Objective To investigate the relationship among the concentration of plasma interleukin (IL)-10 and plasma IL-13 and the clinical therapeutic effect in patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD).Methods Thirty-six AECOPD inpatients were enrolled in this study.Blood samples of the subjects were collected as soon as hospitalization, and plasma IL-10 and IL-13concentrations were analyzed by enzyme-linked immunosorbent assay.The clinical manifestations of subjects were quantified by a special designed score standard, and were evaluated at the time points of hospitalization, 48 hours treatment and 96 hours treatment.The therapeutic effect was evaluated by clinical manifestations score combined with pulmonary ventilation functional parameter.Eventually, the correlation among the concentration of IL-10 concentration and IL-13 and the clinical therapeutic effect were analyzed.Results The correlation coefficients between clinical manifestations score decrease and pulmonary ventilation function improvement with plasma IL-10 concentration after 48 hours treatment were 0.85 and 0.48 respectively,then, 0.64 and 0.52 after 96 hours treatment.The correlation coefficients between clinical manifestations score decrease and pulmonary ventilation function improvement with plasma IL-13 concentration after 48hours treatment were -0.41 and -0.34, after 96 hours treatment , correlation coefficients between clinical manifestations score decrease with plasma IL-13 concentration was -0.36.All of the above correlation coefficients were statistically significant.Conclusion Plasma IL-10 concentration was positively, whereas, IL-13 concentration was negatively correlated with the therapeutic effect in AECOPD patients.

SELEX is a newly developed biochemical technique,which filter out high specificity and high affinity ligand for the target molecules through the identification of aptamer combined with the target molecules.The specific aptamer was used in a variety of clinical applications,such as diagnosis of the disease,development of new therapeutic drugs and even directly applied to disease treatment.

Objective To investigate the molecular mechanism of vascular endothelial growth factor ( VEGF) expression in bronchial epithelial cells (Beas-2B)induced by particulate matter 2.5(PM2.5).Methods PM2.5 powder was dis-solved in DMEM medium and diluted into five concentrations , 0,12.5,25,50 and 100μg/ml, respectively.The double an-tibiotics ( streptomycin and penicillin ) and FBS were added into the solution to a 2% final concentration of serum system after being treated by ultrasound for 30 minutes.The cultured Beas-2B cells were then treated with different doses of PM2.5.Subsequently, nuclear factor-kappa B(NF-κB) transactivity and the transcriptional activation of vegf gene promot-er were tested by dual-luciferase reporter gene analysis system while phosphorylation of p 65 , expression levels of IκBαand VEGF were detected by Western blotting .Results PM2.5 induced up-regulation of VEGF expression in Beas-2B cells in a dose-dependent manner , accompanied by NF-κB transactivation at the highest level under 100 μg/ml of PM2.5 treatment. Moreover, PM2.5 induced degradation of the repressor protein IκBαand increase in the phosphorylation level of p 65 sub-unit in Beas-2B cells.Knockdown of NF-κB p65 expression significantly inhibited vegf gene promoter transcriptional activa-tion as well as VEGF protein expression in Beas-2B cells induced by PM2.5.Conclusion PM2.5 induces VEGF expres-sion via activation of NF-κB pathway in bronchial epithelial cells .

Objective To investigate the effect of liver depression (Liver Qi Stagnation) on Th17,Treg,IL-17,IL-10 and airway inflammation in asthmatic rats,and to clarify the immune mechanism of asthma with liver depression.Methods Established the combined with disease and syndrome model of asthma with liver depression.Collected the bronchoalveolar lavage fluid (BALF) to count the total and differential cell.Lung tissue was observed in microscope; the proportion of Th17 cells and Treg cells of CD4 +T cells in peripheral blood was measured by flow cytometry; the levels of IL-17 and IL-10 were determined by ELISA.Results The total number of inflammatory cells[(96.86±4.43)× 107/L,(88.22±3.22)× 107/L],the proportion of eosinophils [(27.58 ±4.65) ％,(22.67±2.43) ％],Th17 cells[(6.86±0.98) ％,(6.01 ±0.77) ％] and IL-17 level [(48.88± 8.06)pg/ml,(43.24± 6.32) pg/ml] of asthma in liver depression group and asthma group were significantly higher than the control group [(30.58 ± 2.49) × 107/L,(0.78 ± 0.12) ％,(2.80± 0.82) ％,(24.11 ±3.40)pg/ml]; Treg cells [(3.09±0.55) ％,(3.96±0.66) ％] and IL-10 level [(19.79±2.80) pg/ml,(20.29±3.12) pg/ml] were significantly lower than the control group [(8.02± 1.26) ％,(30.79 ± 4.01) pg/ml].The total number of inflammatory cells (96.86 ±4.43) × 107/L,the proportion of eosinophils (27.58±4.65) ％ and Th17 cells(6.86±0.98) ％ and IL-17 level (48.88±8.06)pg/mL of asthma in liver depression group were significantly higher than the asthma group (88.22 ± 3.22) × 107/L,(22.67 ± 2.43) ％,(6.01 ± 0.77) ％,(43.24 ± 6.32) pg/ml;the proportion of Treg cells (3.09 ±0.55)％ was significantly lower than the asthma group (3.96± 0.66)％; and the lung histopathology symptoms was more severe than asthma group.Conclusion Liver Qi Stagnation can promote the inflammation of asthma,the imbalance of Th17/Treg and IL-17 level to aggravate the asthma.Liver depression is one of the major internal factors in recurrent episodes of asthma.

Objective To explore the role of the transcriptional factor activator protein (AP)-1 in mediating vascular endothelial growth factor ( VEGF) expression in human bronchial epithelial cells exposed to PM 2.5.Methods Beas-2B cells was treated with PM2.5.Luciferase assay was used to detect the activation status of AP-1 and transcription of VEGF in the Beas-2B cells.The induced activation of c-Jun, ATF2 and VEGF expression was tested by Western blotting assay.Results PM2.5 induced transactivation of the transcriptional factor AP-1, accompanied by phosphorylation of the AP-1 components, c-Jun and ATF2 in Beas-2B cells.Moreover, when AP-1 activation was inhibited by knocking down c-Jun or ATF2 expressions, induction of VEGF expression was partially attenuated in Beas-2B cells.Conclusion AP-1 is a critical transcriptional factor in mediating PM2.5-induced VEGF expression and inflammatory responses in human bronchial epithelial cells.

Objective To investigate the effect of recombinant Vibrio vulnificus hemolysin (rVvhA) on the expression of nitric oxide(NO) and induced nitric oxide synthase(iNOS) in J774A. 1 cells.Methods The inhibitory effect of rVvhA on J774A. 1 proliferation was measured by MTF colorimetry technique. The content of nitrite in culture medium was determined by Griess reagent. The expression of iNOS protein and mRNA were measured by immunofluorescence and RT-PCR, respectively. Results The viability of J774A. 1 cells was apparently inhibited when exposed to 0.8 HU/ml rVvhA and up. With the help of IFN-γ, the expression of NO and the activity of iNOS in J774A. 1 cells were remarkably increased when exposed to 0.4 HU/ml rVvhA. Conclusion rVvhA can increase the expression of NO and iNOS, it may play an important role in the pathogenic mechanism of Vibrio vulnificus.