Entrustable Professional Activities for Chinese Standardized Residency Training in Pediatric Intensive Care Medicine.

Background: Entrustable professional activities (EPAs) were first introduced by Olle ten Cate in 2005. Since then, hundreds of applications in medical research have been reported worldwide. However, few studies discuss the use of EPAs for residency training in pediatric intensive care medicine. We conducted a pilot study of EPA for pediatric intensive care medicine to evaluate the use of EPAs in this subspecialty. Materials and Methods: A cross-sectional study was implemented in pediatric intensive care medicine standardized residency training at the Qilu Hospital of Shandong University. An electronic survey assessing EPA performance using eight scales composed of 15 categories were distributed among residents and directors. Results: A total of 217 director-assessment and 44 residents' self-assessment questionnaires were collected, both demonstrating a rising trend in scores across postgraduate years. There were significant differences in PGY1-vs.-PGY2 and PGY1-vs.-PGY3 director-assessment scores, while there were no differences in PGY2-vs.-PGY3 scores. PGY had a significant effect on the score of each EPA, while position significantly affected the scores of all EPAs except for EPA1 (Admit a patient) and EPA2 (Select and interpret auxiliary examinations). Gender only significantly affected the scores of EPA6 (Report a case), EPA12 (Perform health education), and EPA13 (Inform bad news). Conclusion: This study indicates that EPA assessments have a certain discriminating capability among different PGYs in Chinese standardized residency training in pediatric intensive care medicine. Postgraduate year, gender, and resident position affected EPA scores to a certain extent. Given the inconsistency between resident-assessed and director-assessed scores, an improved feedback program is needed in the future.

IL-25 promotes Th2 immunity responses in airway inflammation of asthmatic mice via activation of dendritic cells.

Allergic asthma occurs as a consequence of inappropriate immunologic inflammation to allergens and characterized by Th2 adaptive immune response. Recent studies indicated that interleukin (IL)-25, a member of the IL-17 cytokine family, had been implicated in inducing Th2 cell-dependent inflammation in airway epithelium and IL-25-deficient mice exhibit impaired Th2 immunity responses; however, how these cytokines influence innate immune responses remains poorly understood. In this study, we used ovalbumin (OVA) sensitization and challenge to induce the murine asthmatic model and confirmed by histological analysis of lung tissues and serum levels of total and OVA-specific immunoglobulin (Ig)-E. The expression of IL-25 was detected by quantitative real-time PCR and immunohistochemistry, respectively, and the dendritic cells (DCs) activation was detected by levels of CD80 and CD86 in bronchoalveolar lavage fluid (BALF) by flow cytometry. The mice sensitized and challenged with OVA showed high expression of IL-25 in both mRNA and protein levels in lungs. We detected the expression of CD80 and CD86 in BALF was also increased. A tight correlation between IL-25 mRNA and other Th2 cells producing cytokines such as IL-4, IL-5, and IL-13 in BALF was identified. Furthermore, when the asthmatic mice were treated with inhaled corticosteroids, the inflammatory cells infiltration and the inflammatory cytokines secretion were significantly decreased. In this study, we show that IL-25 promoted the accumulation of co-stimulatory molecules of CD80 and CD86 on DCs and then induced the differentiation of prime naive CD4(+) T cells to become proinflammatory Th2 cells and promoted Th2 cytokine responses in OVA-induced airway inflammation. The ability of IL-25 to promote the activation and differentiation of DCs population was identified as a link between the IL-17 cytokine family and the innate immune response and suggested a previously unrecognized innate immune pathway that promotes Th2 cytokine responses in asthmatic airway inflammation. Inhaled corticosteroids might be capable of inhibiting the promotion of IL-25 and present a promising strategy for the treatment of asthma.

House dust mite regulate the lung inflammation of asthmatic mice through TLR4 pathway in airway epithelial cells.

Aberrant innate and adaptive immune responsed to allergens and environmental pollutants lead to respiratory allergic disease such as asthma. In this study, we focused on toll-like receptor-4 (TLR4) expressed on airway epithelium to identify house dust mite (HDM)-regulated allergic inflammation via TLR4 signaling pathway and the triggering to alveolar macrophages (AM)-driven adaptive immune response. The authors found that mouse exposed to HDM showed more eosinophils, neutrophils, monocytes, lymphocytes as well as total cells in bronchoalveolar lavage fluid (BALF) confirmed by flow cytometry. Besides, the expression of TLR4 in airway epithelial cells was significantly increased in both mRNA and protein levels in mice treated with HDM and the expression of CD40 and CD86 in AM was also increased in mice exposed to HDM. Tight correlation between TLR4 protein and CD40, CD86 in AM was identified. This study demonstrates that TLR4 expression on airway epithelium played an essential role in HDM-induced activation of AM in immune responses and allergic inflammation. The airway epithelial TLR4 signaling pathway revealed tight connection between endotoxin exposure and asthma prevalence in the clinic.

Anti-inflammatory and antiallergic effects of polysaccharide nucleic acid fraction of bacillus calmette guerin / 中国药理学通报

Aim To study the anti-inflammator y and antiallergic effects of polysaccharide nucleic acid fraction of bacillus cal mette guerin (BCG-PSN). Methods Effect of BCG-PSN on itch thr eshold of guinea pigs caused by phosphoric acid histamine, ear oedema of mice ca used by xylene, carrageenan-induced hind paw oedema in rats, delayed hypersensi tivity reaction induced by 2,4-dinitroflurobenzene in mice, homologous passive cutaneous anaphylaxis in rats and heterologous passive cutaneous anaphylaxis in mice were investigated. BCG-PSN was administered intramuscularly every other d ay for three weeks. Results BCG-PSN(0.1,0.2,0.4 mg?kg -1) had no effect on itch threshold of guinea pigs caused by phosphoric aci d histamine. In mice, BCG-PSN(0.15,0.30,0.60 mg?kg -1) significant ly inhibited ear oedema caused by xylene and heterologous passive cutaneous anap hylaxis in a dose-dependent manner. BCG-PSN at the dose of 0.60 mg?kg -1 also significantly inhibited delayed hypersensitivity reaction induced by 2,4 -dinitroflurobenzene in mice. In rats, BCG-PSN(0.1,0.2,0.4 mg?kg -1 )significantly inhibited carrageenan-induced hind paw oedema and homologous passive cutaneous anaphylaxis. Conclusion BCG-PSN inhibites ac ute inflammation, immediate type allergy and delayed type allergy.

Experimental evaluation of the antihistamine effect of domestic azelastine hydrochloride / 中国临床药理学与治疗学

AIM: To evaluate the antihistamine effects of domestic azelastine hydrochloride. METHODS: Histamine increased skin vascular permeability and induced shock model in guinea pigs. In isolated guinea pig ileal rings, the contraction of smooth muscle induced by histamine was determined. RESULTS: Pretreament with azelastine hydrochloride( 0.05, 0.15,and 0.45 mg?kg -1,ig) significantly inhibited the increase in skin vascular permeability induced by histamine in a dose-dependent manner in guinea pigs. Pretreament with azelastine hydrochloride( 0.05, 0.1,and 0.2 mg?kg -1,ig)produced a significant improvement of shock, as shown by a decrease in reactivity degree, mortality and a prolongation of latency. In isolated guinea pig ileal rings, azelastine hydrochloride (10 -8,3?10 -8,10 -7,3? 10 -7 mol?L -1)significantly inhibited contraction of smooth muscle induced by histamine in a concentration-dependent manner and caused a parallel right shift of the dose-effect curve of histamine (pA 2= 8.55). CONCLUSION: Domestic azelastine hydrochloride shows significant the antihistamine effects.