Objective: To explore the expression of Eotaxin and the effect of histamine in allergic rhinitis model (AR),and aim to explore the pathogenesis of AR. Method:The AR models were established by applicating of ovain albumin in rats. The expression of Eotaxin in nosal mucosa,serum and nasal cavity lavage fluid,were observed before and after treatment of histamine or its antagonist by immunochemistry,RT-PCR and ELISA technique. Result:The expression of Eotaxin in nasal lavage fluid and nasal mueosa increased after treatment of histamine(P＜0.05). Contrarily,the expression of Eotaxin in nasal lavage fluid,nasal mucosa and serum decreased after treatment of the antagonist of histamine. Conclusion:Both histamine and its receptor can involve in the pathogenesis of AR by affecting the expression of Eotaxin.

Objective To evaluate the protective effect on lung by using continuous pulmonary artery perfusion with oxygenated blood and L-arginine during cardiopulmonary bypass(CPB).Methods Forty five cases received mitral valve replacement were randomly divided into 3 groups and each group involved 15 cases. Group I(control group), patients received routine procedure of CPB. Proup Ⅱ, patients received rcontinuous pulmonary artery perfusion with oxygenated blood. Group Ⅲ,continuous pulmonary artery perfusion with oxygenated blood containing L-arginine (200 mg/kg) (n=15). All cases received routine procedure of CPB and continuously infused from the root of pulmonary artery until releasing aortaoaic clamp. Blood samples were collected from the radial artery respectively at the following time points:after the induction of anaesthesia, 1 hour after opening of aorta, 0, 6, 12, 24 hours after patients being taken back to ICU. ELISA test was used to detected the expression of tmmor necrosis factor-α(TNF-α), interleukin-6 (IL-6) and interleukin-10 (IL-10). Lung tissue samples (1.0 cm ×1.0 cm×1.0 cm) were obtained from right lower lobe. The pathologicl changes of lung tissues were observed under light mi-croscope by using HE staining. Results at each time points, the expression of TNF-α, IL-6 in group Ⅱ and group Ⅲ weresignificantly lower than that in group Ⅰ (P<0.05). The level of TNF-α, IL-6 in group Ⅲ were lower than in group Ⅱ(P<0.05). However, the expression of IL-10 in group Ⅱ and group Ⅲ were higher than in group Ⅰ, and the level of IL-10 in group Ⅲ were higher than that in group Ⅱ(P<0.05). In the group Ⅰ: HE staining showed marked pulmonary interstitial edema, intra-alveolus neutrophilic granulocyte exudation with karyorrhexis. In the group Ⅱ, light capillary vessel hyperaemia and pulmonary interstitial lymphocyte exudation were detected. Nearly normal lung tissue were observed in group Ⅲ. Conclusion Continuous pulmonary artery perfusion with oxygenated blood and L-arginine could inhibit the synthesis of inflammatory factors significantly and increase the releasing of anti-inflammatory factors during CPB. Therefore, it may reduces pulmonary inflammatory reaction and have protective effects on lung tissue.

OBJECTIVE: To explore the expression of Eotaxin and the effect of histamine in allergic rhinitis model (AR), and aim to explore the pathogenesis of AR. METHOD: The AR models were established by application of ovum albumin in rats. The expression of Eotaxin in nasal mucosa, serum and nasal cavity lavage fluid, were observed before and after treatment of histamine or its antagonist by immunochemistry, RT-PCR and ELISA technique. RESULT: The expression of Eotaxin in nasal lavage fluid and nasal mucosa increased after treatment of histamine (P < 0.05). Contrarily, the expression of Eotaxin in nasal lavage fluid, nasal mucosa and serum decreased after treatment of the antagonist of histamine. CONCLUSION Both histamine and its receptor can involve in the pathogenesis of AR by affecting the expression of Eotaxin.
Animals ; Chemokine CCL11 ; biosynthesis ; metabolism ; Female ; Histamine ; metabolism ; Male ; Nasal Mucosa ; metabolism ; Rats ; Rats, Sprague-Dawley ; Rhinitis, Allergic, Perennial ; metabolism ; pathology ; Rhinitis, Allergic, Seasonal ; metabolism ; pathology

Objective · To investigate the clinical characteristics of initial peritoneal dialysis (PD) patients with different peritoneal transport status, and analyze risk factors of high peritoneal transport status in PD patients. Methods · A total of 455 consecutive PD patients newly starting PD between January 2007 to October 2015 were retrospectively analyzed. According to the results of the first sPET, patients were divided into H/HA (4h D/Pcr ≥ 0.65) and L/ LA (4h D/Pcr<0.65) groups. Clinical and biochemical characteristics between the two groups were compared. Multivariate logistic regression model was established to investigate risk factors of higher peritoneal transport status of incident PD patients. Results · The study included 372 incident PD patients. The L/LA group and H/HA group had 264 cases (71.2%) and 108 cases (28.8%) respectively. The H/HA group had higher proportion of male patients (63.0% vs 50.8%, P=0.03), lower residual renal function [RRF, (4.26±2.77) mL/min vs (5.79±4.53) mL/min, P<0.01], lower serum albumin level [(29.34±6.89) g/L vs (32.08±5.86) g/L, P=0.00], and more frequent diabetic nephropathy (19.4% vs 9.5%, P=0.00), compared with L/LA group. Univariate and multivariate logistic regression analysis showed that higher peritoneal transport status was associated with lower serum albumin level (OR=0.96, 95% CI 0.28-0.99; P=0.02), male (OR=1.92, 95% CI 1.19-3.12; P=0.00), presence of diabetic nephropathy (OR=2.52, 95% CI 1.26-5.05; P=0.00) and lower residual renal function (OR=0.90,95% CI 0.83-0.96; P=0.00). The level of hsCRP in patients with hypoalbuminemia was higher than that in patients with normal albumin level (1.69 mg/L vs 0.69 mg/L, P=0.00). Conclusion · Low and low average peritoneal transport status accounted for the majority of the patients in this study. Low serum albumin levels, male, diabetic nephropathy, RRF were risk factors of initial high peritoneal solute transport status. Chronic inflammatory status might partially explain for the correlation between hypoalbuminemia and high peritoneal solute transport status in PD patients.

OBJECTIVE: To study the change of endogenous hydrogen sulfide (hydrogen sulfide, H2S) and its rate-limiting enzyme Cystathionine-gamma-lyase (CSE) in allergic rhinitis through guinea pigs with intervention treatment. METHOD: Twenty-four guinea pigs were divide into 4 groups at random, one group were models of allergic rhinitis (AR) which were established by using ovalbumin, the second group were treated with NaHS after sensitized, the third group were treated with Propargylglycine (PPG) which was suppression of CSE after sensitized, and the last group were treated with saline for control. The concentration of eotaxin of nasal lavage and H2S in plasma were recorded, and then the expression of CSE in nasal mucosa was determined by real-time fluorescence RT-PCR. RESULT: The concentration of eotaxin in nasal lavage of sensitized group were higher than those of control (P < 0.01), and concentration of H2S in plasma and expression of CSE in nasal mucosa were lower than control (P < 0.05). The concentration of eotaxin decreased when treated with NaHS and increased when treated with PGG (P < 0.05). Level of H2S in plasma and expression of CSE increased when treated with NaHS and decreased when treated with PGG (P < 0.05), and the level of H2S was positive linear correlate with the expression of CSE. CONCLUSION Endogenous H2S perhaps plays a significant role in the pathogenesis of allergic rhinitis, and it was mainly regulated by CSE.
Animals ; Cystathionine gamma-Lyase ; metabolism ; Guinea Pigs ; Hydrogen Sulfide ; metabolism ; Male ; Nasal Mucosa ; metabolism ; Rhinitis ; metabolism

PURPOSE: Allergic rhinitis (AR) is an inflammatory disorder of the upper airway. Exosomes or extracellular vesicles are nanosized vesicles of endosomal origin released from inflammatory and epithelial cells that have been implicated in allergic diseases. In this study, we characterized the microRNA (miRNA) content of exosomes in AR. METHODS: Extracellular vesicles were isolated from nasal mucus from healthy control subjects (n=10) and patients with severe AR (n=10). Vesicle RNA was analyzed by using a TaqMan microRNA assays Human Panel-Early Access kit (Applied Biosystems, Foster City, CA, USA) containing probes for 366 human miRNAs, and selected findings were validated with quantitative RT-PCR. Target prediction and pathway analysis for the differentially expressed miRNAs were performed using DIANA-mirPath. RESULTS: Twenty-one vesicle miRNAs were up-regulated and 14 miRNAs were under-regulated significantly (P<0.05) in nasal mucus from AR patients when compared to healthy controls. Bioinformatic analysis by DIANA-mirPath demonstrated that 32 KEGG biological processes were significantly enriched (P<0.05, FDR corrected) among differentially expressed vesicle miRNA signatures. Among them, the B-cell receptor signaling pathway (P=3.709E-09), the natural killer cell-mediated cytotoxicity (P=8.466E-05), the T-cell receptor signaling pathway (P=0.00075), the RIG-I-like receptor signaling pathway (P=0.00127), the Wnt signaling pathway (P=0.00130), endocytosis (P=0.00440), and salivary secretion (P=0.04660) were the most prominent pathways enriched in quantiles with differential vesicle miRNA patterns. Furthermore, miR-30-5p, miR-199b-3p, miR-874, miR-28-3p, miR-203, and miR-875-5p, involved in B-cell receptor and salivary secretion signaling pathways, were selected for validation using independent samples from 44 AR patients and 20 healthy controls. MiR-30-5p and miR-199b-3p were significantly increased in extracellular vesicles from nasal mucus when compared to healthy controls, while miR-874 and miR-28-3p were significantly down-regulated. In addition, miRNA-203 was significantly increased in AR patients, while miRNA-875-5p was found to be significantly decreased in AR patients. CONCLUSIONS: This study demonstrated that vesicle miRNA may be a regulator for the development of AR.
B-Lymphocytes ; Biological Processes ; Endocytosis ; Epithelial Cells ; Exosomes ; Humans ; MicroRNAs* ; Mucus* ; Receptors, Antigen, T-Cell ; Rhinitis* ; RNA ; Wnt Signaling Pathway