As a heteronomy,the code of medical ethics plays an important role in sustaining the trust between physicians and patients.Based on a comparative analysis of the domestic and foreign codes of medical ethics,and field survey on such trust at tertiary hospitals in Beijing,as well as medical providers’moral characteristics,this article analyzed the causes that “goodwill”is insufficient in the trust in terms of internal and external factors;and then,in respect of heteronomy as a basis,it put forward suggestions to improve code of medical ethics in order to rebuild such trust.

Objective:To observe the changes in percentages and subsets of invariant nature kiler T (iNKT) cells in adipose and related tissues at different stages of obesity, and analyze the role of iNKT cells during chronic inflammation in adipose tissues in a mouse model of obesity established with high-fat diet.Methods:Changes in mouse body weight, mental state, glucose tolerance and insulin tolerance were recorded. Hematoxylin and eosin (HE) staining was used to observe pathological changes in adipose tissues. Flow cytometry was performed to detect the percentages and subsets of iNKT cells as well as the percentages and subtypes of macrophages. The levels of cytokines in serum samples and the culture supernatants of lymphocytes in adipose tissues were detected with CBA. The expression of related proteins in adipose tissues was detected by Western blot.Results:(1) The volume of adipose cells increased significantly after four weeks of high-fat feeding, but the infiltration of inflammatory cells was not obvious. Significantly increased infiltration of inflammatory cells was observed after 12 weeks of high-fat feeding. (2) High-fat feeding could reduce the percentage of iNKT cells, increase the proportion of iNKT1 subgroup and decrease the proportion of iNKT10 subgroup in adipose tissues. The proportion of iNKT1 subgroup in thymus increased, but that of iNKT2 subgroup decreased. The percentage of macrophages and the proportion of M1 subgroup in adipose tissues increased, while the proportion of M2 subgroup decreased, which were more obvious after 12 weeks of high-fat feeding. (3) High-fat feeding resulted in decreased expression of E4BP4 and arginase-1 (Arg-1) in adipose tissues and increased expression of inducible nitric oxide synthase (iNOS). (4) High-fat feeding significantly increased the pro-inflammatory cytokines and decreased the anti-inflammatory cytokines in mouse serum and culture supernatants of lymphocytes in adipose tissues with more significant changes observed after 12 weeks of high-fat feeding.Conclusions:Increased iNKT1 and decreased iNKT10 in obese adipose tissues might be closely related to the increased M1 polarization and the imbalance of iNKT subsets might be involved in the progression of chronic inflammation in obese adipose tissues.

Objective:To investigate the risk factors of dysplasia in patients with ulcerative colitis (UC) in China.Methods:From March 1st, 2012 to December 30th, 2013, a total of 154 UC patients were prospectively enrolled from the following 11 hospitals, Xijing Hospital of Digestive Diseases, Ruijin Hospital affiliated to Shanghai Jiao Tong University School of Medicine, Peking Union Medical College Hospital, Renji Hospital affiliated to Shanghai Jiao Tong University School of Medicine, Nanfang Hospital affiliated to Southern Medical University, China-Japan Friendship Hospital, The Second Hospital of Hebei Medical University, West China Hospital affiliated to Sichuan University, The Seventh Medical Center of PLA General Hospital, Zhongshan Hospital affiliated to Xiamen University, and the First Affiliated Hospital of Anhui Medical University. The patients were followed up till December 1st, 2017. All the UC patients underwent colon endoscopy and histopathological evaluation. T test and Chi-square test were used for statistical analysis. Cox proportional risk model was used for identifying the risk factors of dysplasia in UC patients. Results:Finally, 133 UC patients were enrolled, the age was (50.0±11.9) years, the diagnosis age was (35.5±11.6) years, the course of disease was (14.5±6.7) years, and the number of endoscopic examinations was (3.4±1.6) times. A total of 21 patients were detected with dysplasia. No patients were detected with colorectal cancer. The results of univariate analysis revealed that the diagnosis age (hazard ratio ( HR)=1.05, 95% confidence interval ( CI) 1.01 to 1.10, P=0.009) and extensive colitis ( HR=2.92, 95% CI 0.97 to 8.79, P=0.057) were factors with statistically significant difference. The results of multivariate analysis revealed that the old age at diagnosis ( HR=1.06, 95% CI 1.02 to 1.11, P=0.003) and extensive colitis ( HR=3.68, 95% CI 1.21 to 11.19, P=0.022) were independent risk factors of dysplasia in UC patients. The cumulative incidence of dysplasia of UC patients with extensive colitis was higher than that of patients with left-sided colitis (24.3%, 17/70 vs. 6.3%, 4/63), and the difference was statistically significant ( χ2=8.023, P=0.005). Conclusions:Extensive colitis and older age at diagnosis are two independent risk factors of dysplasia in UC patients of our country. The cancer monitoring should be strengthened in UC patients with long course of disease and extensive colitis.

OBJECTIVETo investigate the role of miR-199a-3p in cardiac fibrosis and the potential target of miR-199a-3p.

METHODSCardiac fibroblasts were isolated from C57BL/6 mice and cultured. The miR-199a-3p mimic and Smad1 siRNA were transiently transfected into the cardiac fibroblasts via liposome. Dual luciferase reporter assay was performed to confirm the interaction between miR-199a-3p and the 3'-UTR of Smad1. The expressions of Smad1 and fibrosis-related genes at the mRNA and protein levels in the cells after miR-199a-3p mimic transfection were determined using RT-qPCR and Western blotting, respectively. The expressions of Smad1, Smad3 and fibrosis-related genes at the protein level in cells transfected with miR-199a-3p mimic and Smad1 siRNA were detected using Western blotting.

RESULTSOver-expression of miR-199a-3p significantly increased the expression of cardiac fibrosis-related genes in cultured mouse cardiac fibroblasts. Dual luciferase reporter assay revealed the interaction of miR-199a-3p with the 3'-UTR of Smad1. The results of RT-qPCR and Western blotting confirmed that miR-199a-3p inhibited Smad1 expression at the post- transcriptional level. Transfection with miR-199a-3p mimic and siRNA-mediated Smad1 silencing consistently activated the Smad3 signaling pathway and enhanced the expressions of cardiac fibrosis-related genes in the cardiac fibroblasts.

CONCLUSIONSAs the target gene of miR-199a-3p, Smad1 mediates the pro-fibrotic effect of miR-199a-3p by activating the Smad3 signaling in cultured mouse cardiac fibroblasts.

Objective    To analyze the factors influencing the occurrence of subclinical leaflet thrombosis (SLT) after percutaneous aortic valve replacement using balloon-expandable valve (Sapien3, S3). Methods     Retrospective analysis was made on 62 patients with severe aortic stenosis undergoing percutaneous aortic valve replacement using S3 in our center from September 2020 to June 2022. Patients with a history of vascular atherosclerosis or with significant increase or insignificant decrease of aortic valve flow or gradient pressure during follow-up were selected for CT examination. Results     A total of 26 patients were finally included, with an average age of 70.31±8.90 years, and the male proportion was higher (n=15, 57.69%). Among them, 5 patients had SLT. Compared with the non-SLT group, patients in the SLT group were older (68.52±8.80 years vs. 77.80±4.66 years, P=0.007). The age factor (≥75 years) and the diameter of the ascending aorta were associated with SLT (both P<0.05). Conclusion     The incidence of SLT is higher in the elderly patients. It is speculated that SLT is related to the characteristics of short balloon dilation valves and low blood flow dynamics of valve racks.