Mast cells (MCs) play a key role in the pat hogenesis of allergic diseases. Tissue MCs are originated from hematopoietic ste m cells in bone marrow. In recent years, it was reported that human mast cells c ould be differentiated from stem cells of umbilical cord blood. In this review, we summarize the development in this novel area.

AIM: To investigate the actions of trypsi n on the secretion of monocyte chemoattractant protein-1 (MCP-1) from human lung e pithelial cells. METHODS: A549 cells were cultured in a 12-well culture plate. Th e challenge was performed by addition of various concentrations of trypsin or tr ypsin inhibitor into each well, respectively. After 2 h, 8 h or 16 h, the reacti ons were terminated by removal of the supernatant from each well. A sandwich ELI SA was used to determine the levels of MCP-1 in supernatants. RESULTS: Following 16 h incubation, trypsin was able to induce c oncentration-dependent secretion of MCP-1. As low as 3 ?g/L trypsin was able to induce MCP-1 release from epithelial cells, and the maximum of accumulated rele ase of MCP-1 was observed with 100 ?g/L trypsin, which was 3 fold more than bas eline release. However, trypsin at 300 ?g/L did not induce significant MCP-1 se cretion. Soybean trypsin inhibitor (SBTI) inhibited trypsin-induced MCP-1 secret ion, but ? 1-antitrysin (? 1-AT) did not. The time course showed that the actions of trypsin initiated at 2 h and reached their peak at 16 h. CONCLUSION: Trypsin is a potent secretogogue of MCP-1 release fr om cultured human lung epithelial cells, and itself action can be inhibited by S BTI.

Objective To investigate the risk factors that worsened the pathologic course of acute ischemic stroke .Methods The clinical data of 264 patients with acute ischemic stroke treated in Shijitan hospital were analyzed retrospectively .According to the outcome ,the patients were divided into deterioration group (70 cases) and improved group(194 cases) .The clinical data ,labora-tory examination results of the patients were collected through self-made survey and compared between the two groups .The risk factors that worsened the pathologic course of acute ischemic stroke were analyzed by multiple linear regression .Results There were 42 .86% patients with hyperlipidemia history and 70 .00% with diabetes history in the deterioration group ,which were signifi-cantly higher than the improved group(P<0 .05) .The levels of glucose ,glycosylated hemoglobin ,fibrinogen ,serum ferritin ,C reac-tive protein ,low density lipoprotein cholesterol in the deterioration group were significantly higher than those in the improved group (P<0 .05) .Multiple linear regression analysis showed that hyperlipidemia history ,high level of C reactive protein ,and high level of low density lipoprotein cholesterol were the independent risk factors that worsened the pathologic course of acute ischemic stroke . Conclusion Hyperlipidemia history ,high level of C reactive protein ,and high level of low density lipoprotein cholesterol were the independent risk factors that worsened the pathologic course of acute ischemic stroke .According to these factors ,patients were e-valuated and targeted measures were made to improve the prognosis of the patients .

Objective To investigate the actions of PAR1 agonists and thrombin on the secretion of monocyte chemoattractant protein (MCP)-1 from human lung epithelial cells. Methods A549 cells were cultured in a 12-well culture plate. The challenge was performed by addition of various concentrations of PAR1 agonist peptides SFLLR and its reverse peptides RLLFS, thrombin or thrombin inhibitor named hirudin into each well, respectively. After 2 h or 16 h, the reactions were terminated by removal of the supernatant from each well. A sandwich ELISA was used to determine the levels of MCP-1 in supernatants. Results Following 16 h incubation, SFLLR could induce concentration-dependent secretion of MCP-1. The maximum release of MCP-1 was nearly 12-fold more than baseline release. The reverse PAR1 agonists had little effects on MCP-1 release. Thrombin could induce concentration-dependent secretion of MCP-1. As low as 3 000 U/L thrombin could induce MCP-1 release from epithelial cells, and the maximum of accumulated release of MCP-1 was observed with 10 000 U/L thrombin, which was 5-fold more than baseline release. Thrombin inhibitor hirudin could inhibit thrombin induced secretion of MCP-1. The time course showed that the actions of PAR1 agonist peptides SFLLR and thrombin initiated at 2 h and reached their peak at 16 h. Conclusion PAR1 agonist peptides and thrombin are potent secretogogue of MCP-1 release from cultured human lung epithelial cells, and PAR1 antagonists and thrombin inhibitor may possess the ability to inhibit airway inflammation.

Objective To investigate the potential influence of TNF on the expression of protease activated receptor (PAR)-1,2,3 and 4 by using P815 mast cells. Methods After being challenged with various concentrations of TNF for 2 h, 6 h and 16 h, the P815 mast cells were treated with or without Triton X-100 and the PAR expressions were detected by flow cytometry and immunofluorescent microscopy. Results Compared with the corresponding controls, TNF concentration-dependently upregulated expressions of PAR-2 and PAR-4 both in Triton X-100-treated and the untreated groups, but had no significant effect on the expression of PAR-1 and PAR-3. Moreover, no significantly different expressions of TNF-induced PAR-1, 2, 3 were observed between Triton X-100-treated and the untreated groups, whereas Triton X-100-treated PAR-4 expressions were significantly enhanced by TNF compared with the Triton X-100-untreated ones. Conclusion TNF can up-regulate PAR-2, 4 expression of P815 mast cells but has little effect on the expression of PAR-1, 3 correspondingly. And Triton X-100 treatment had no significant effect on TNF-modulated expression of PARs in P815 mast cells.

Objective To study the expression of Adiponectin (AD) and its receptors Adiponectin receptor 1 (Adipo R1) and Adipo R2 in the synovial fluids and the synovium of rheumatoid arthritis (RA). Methods ELISA was used to determine the levels of AD in 23 RA and 23 osteoarthritis (OA) patients. Real-time PCR and Western blot techniques were employed to study the expression of AD, AdipoR1 and AdipoR2 in the synovium of 10 RA and OA patients. Results It was observed that approximately twice more adiponeetin in the synovial fluids of patients with RA than with OA. Adiponectin and AdipoR1, but not AdipoR2 mRNA, were significantly expressed in synovium of RA patients in comparison with OA. Adiponectin and AdipoR1 protein were wuch more expressed in synovium from RA than those from OA. Conclusion High expression of Adiponectin and AdipoRl is likely to contribute to the formation of inflammatory joints in RA.

BACKGROUND:Early detection and accurate staging diagnosis of heart failure are the basis of good clinical therapy efficacy. Due to lack of simple and effective staging model for the diagnosis of heart failure, it is difficult to diagnose heart failure in clinics, leading to poor control of heart failure. OBJECTIVE:To establish the disease staging model based on Adaboost and SVM for heart failure, and improve the accuracy of diagnosis and staging of heart failure. METHODS:A total of 194 cases were roled into this study, including heart failure patients and healthy physical examination persons. According to the stage standards formulated by American Colege of Cardiology and American Heart Association, specific clinical feature parameters closely related to heart failure were colected and selected. Based on clinical diagnosis results and using Adaboost model and SVM model, we trained the models for heart failure diagnosis and staging, thus obtaining diagnosis model. RESULTS AND CONCLUSION: The parameters included stroke volume, cardiac output, left ventricular ejection fraction, left atrial diameter, left ventricular internal diameter at end-systole, N-terminal pro-brain natriuretic peptide and heart rate variability. As for the Adaboost model, its sensitivity and specificity was 100% and 94.4%, respectively. At the same time the SVM model had good sensitivity and specificity, 86.5% and 89.4% respectively. Adaboost classification model can be accurate in the diagnosis of heart failure symptoms, the accuracy reached 89.36%. On the basis of the diagnosis of heart failure, the SVM classification model is effective in staging the severity of heart failure, staging accuracy for staging B and C was 86.49% and 81.48%, respectively. The findings indicate that, combining Adaboost and SVM machine learning models could provide an accurate diagnosis and staging model for heart failure.

Objective To investigate whether the amount of blood transfusion affects the lengths of stay (LOS),costs,and outcomes of hospital patients or not,and to prepare for the execution of patient blood management.Methods The data of hospital patients,who had been administrated with blood in our hospital during 2016,were collected.And the influence of blood transfusion volume on LOS,costs and outcomes of patients was analyzed retrospectively.Results LOS,costs and outcomes of patients vary significantly with the amount of blood transfusion (P＜0.01).There were positive correlations between the total amount of blood transfusion and LOS,costs,and outcomes of patients.The Spearman correlation coefficient was 0.317,0.497,0.290,respectively (P＜0.01).Plasma preparation transfusion volume has a great influence on LOS,costs,and outcomes than red blood cell (P＜0.05).The transfusion volume of death patients was significantly higher than that of the survival (P＜0.01).In particular,the amount of transfused plasma and precipitation was distinctly higher than that in death patients(P＜0.01).Conclusion Blood transfusion volume affects LOS,costs and outcomes of hospital patients.The administration of plasma preparations should deserve more attention.

Objective: To observe the clinical efficacy of acellular dermal matrix combined with modified tunnel in the treatment of gingival recessions. Methods: 27 teeth with gingival recessions in 8 patients were treated by the means of acellular dermal matrix and modified tunnel technique and were followed up for 1 year. The clinical parameters of gingival recession depth,recession width,keratinized tissue height,probing depth and clinical attachment level were assessed. Percentage of root coverage(PRC),complete root coverage(CRC) and patient satisfactions were evaluated. Results: 1 years after treatment PRC reached to 76％,19 teeth got complete root coverage. Recession depth and recession width were significantly decreased(P ＜ 0. 05). Keratinized tissue height increased by(1. 25 ± 0. 24) mm. Clinical attachment level increased by(2. 75 ± 0. 59) mm. Conclusion: Acellular dermal matrix allograft combined with modified tunnel technique is effective in the treatment of gingival recessions.

Objective To explore the potential role of high levels of adiponectin (AD) in the inflammatory joint of rheumatoid arthritis (RA). Methods ELISA was used to measure the levels of AD, IL-Iβ,IL-6, IL-8, TNF-α, MCP-1 and MMP-9 in the synovial fluids of RA and osteroarthritis (OA), the levels of these cytokines were tested after the synovial fibroblasts (SFLs) were stimulated with AD. Doublelabeling immunohistochemistry was used to analyze the expression of AD in RA synovium. Cytokines were measured by ELISA after SFLs were stimulated with AD. The expression of RANKL was detected by real-time PCR after MH7A were treated with AD and IL-6 ANOVA, Student's t-test, Mann-Whitney U-tese, Spearman's-test were used for statistical analysis. Results High levels of AD in RA synovial fluids were correlated with IL-6 levels. Double labeling immunohistochemistry showed that AD was localized in fibroblasts. MCP-1 and IL-6 were dramatically increased in human synovial fibroblasts following incubation with recombinant AD for 24 h. RANKL mRNA was significantly increased in MH7A after treated with AD and IL-6. Conclusion High levels of AD in the inflammatory joints of RA are likely to contribute to the high expression of IL-6, MCP-1 and RANKL, which may play an important role in the chronic inflammation, osteoclasts activation and bone erosion in RA.