AIM: To observe the expression of TNF-?, I L-6 mRNA in injured myocardium caused by infectious pneumonia and the effects of exogenous adenosine.METHODS: Fifty rats were divided into five experimental groups at random. The model of pneumonia was replicated by the inj ection of staphylococcus aureus into the windpipe of rats. Adenosine-treated ra ts (A,B and C group) received daily injection of adenosine at different dosages (50, 100 and 150 ?g?kg -1 ?min -1 for 90 min) for 3 days. All rat s were killed on the fifth day. Pathological examination of myocardium were don e and TNF-?, IL-6 mRNA expression were detected by reverse transcription poly m erase chain reaction (RT-PCR). RESULTS: (1) Significant increa se in TNF-?, IL-6 mRNA expression was observed in myocardium of pneumonic rats compared with control group ( P0 05). IL-6 mRNA expression in adenosine-treated C group was lower than that in adenosine-treated B group ( P

Objective To investigate the effect of different adjuvants and challengemethods on asthma mice′s lung inflammation . Methods BALB/c mice were sensitized with ovalbumin in aluminium hydroxide or alum adjuvant .After 7 days challenges ,choose the proper adjuvant with intranasal or atomized to prepare mice asthma model .Count and classify the white blood cells (WBC) in bronchoalveolar lavage fluid(BALF) ,observe the peribronchial and perivascular inflammation .Results Compare the WBC and eos-nophils in BALF ,the alum group are higher than aluminum hydroxide group(P<0 .05) ,5 and 7 days′atomized groups are highter than 3 days′intranasal group(P<0 .05) ,5 and 7 days′atomized groups have showed no significant difference (P>0 .05) .10 days after the last challenge ,the inflammation fade sharply ,and the corresponding result occured in the lung inflammation .Conclusion In establishing asthma model ,alum is better than aluminum hydroxide ,atomization is better than intranasal .Inflammation will fade after stop atomization a period of time .

Objective To understand the infection situation and epidemiological characteristics of Mycoplasma pneumonia (MP) among children with MP infections in Guilin area .Methods The IgM antibody of MP was determined in 1 704 pediatric outpatients and inpatients with respiratory tract infections in our hospital during 2015 by using the MP IgM antibody test reagent kit(colloidal Gold method) .The detection situation was investigated and analyzed .Results The total MP positive rate among children patients with respiratory tract infections in Guilin was 18 .19% ,the female was higher than male with statistical difference (22 .48% vs . 15 .37% ,P<0 .05) .The MP positive rates in children 0 - <1 years old ,1 - <3 years old ,3 - <6 years old and 6 -14 years old were 6 .25% ,18 .59% ,25 .56% and 32 .40% respectively ,and the differences were statistically significant (P<0 .05) .The MP posi‐tive rates in spring ,summer ,autumn and winter were 21 .56% ,15 .29% ,16 .52% and 18 .48% respectively ,and the differences were not statistically significant(P>0 .05) .Conclusion MP is one of the most common pathogens leading to respiratory tract infection in children ,its infection shows gender and age differences .Summer and autumn are mainly epidemic seasons .Children aged 6―14 years old are susceptible to be infected by MP .So it is necessary to strengthen the prevention of MP infection .

Objective To investigate the clinical features of Henoch-Schonlein purpura nephritis(HSPN) and the clinical significance of plasma endothelin-1(ET-1) in HSPN.Methods The epidemiology and clinical characteristics were retrospectively analyzed in 84 patients admitted to our hospital from January 2000 to March 2005.The changes of ET-1 were measured in 84 patients and 16 controls by using radioimmunologic assay.Results The age of onset in HSPN was 5-10 years and the corresponding patients occupied 90.6%.The majority of HSPN cases(80.32%) occurred from September to March of the second year.Infection was still the main occasion factor(40.57%),and the mistaken diagnosis at rate of 33.33% as acute gastricism and appendicitis when gastrointestinal sign appeared earlier than the typical purpura.The nephritic syndrome was the most constant clinical manifestation(47.63%).The pathological type of grade Ⅱ was 37.84%,grade Ⅲ 56.40%.The level of plasma ET-1 in patients was more higher than that of normal controls.The level of plasma ET-1 had a positive correlation with plasma urea nitrogen and creatinine(r=0.584,0.523,P

AIM: We used an animal model of chronic hypoxia to mimic right ventricular hypertrophy and try to study the potential mechanism of myocardium apoptosis of right heart in rat under chronic hypoxia.METHODS: Rat hypoxia models were established by exposing the rats to normobaric chronic hypoxia(oxygen levels were maintained at 9.5%-10.5%).Sixty rats were separated into two groups: one exposed to hypoxia and the other serving as control.Ten rats,randomly selected from each group were killed at 14,21,28 d after hypoxia.The apoptosis was determined.The changes of RV weight to left ventricle and interventricular septum weight ratio[RV/(LV+S)],the RV weight to body weight ratio(RV/BW) were also observed.The ?-MHC,bcl-2 and bad mRNA levels in right ventricle were detected by semi-quantitative RT-PCR assays and expression of ?-MHC,Bcl-2 and Bad protein levels were detected by Western blotting.RESULTS: The RV/(LV+S),RV/BW and apoptosis index in chronic hypoxia group were higher than those in normal control group(P0.05).Finally,a decreased bcl-2/bad ratio in chronic hypoxia group was found compared with control group(P

Objective To observe the effect of PM2.5 on the secretion of NO, ET-1 and the proliferation of rat vascular smooth muscle cell(VSMC) in vitro.Methods VSMCs were treated with PM2.5 collected from urban area of Zhanjiang,at the doses of 10,20,50,100 and 200 ?g/ml.After 24 hours of treatment, the levels of NO and ET-1 in the VSMCs were detected by nitrate reductase method and radioimmunoassay respectively, the proliferation of VSMCs was detected by MTT.Results At the concentrations of 10-200 ?g/ml, with PM2.5 increased, the level of NO in VSMCs decreased from(43.53 ?3.46)?mol/L to(29.28?2.28)?mol/L(F=18.89,P

Objective To explore the effect of calcium gene-related peptide (CGRP) on free calcium concentration in the brain cells of hypoxic-ischemic neonatal SD rats. Methods Animal model of hypoxic-ischemic cerebral injury was set up using SD rats of 7 days old. Then the rats were randomly divided into treatment group given 3?g/kg/d CGRP intraperitoneally for 3 days immediately after the model was made, and salt solution group given 0.9% NaCl solution intraperitoneally for 3 days. Normal control group received sham operation. All the rats were decapitated after 3 days and the concentration of free calcium in brain cells was measured with calcium fluorescence indicator in Fura-2Am. Results The free calcium concentration in brain cells in salt solution group was significantly higher than that in the other two groups (P

Objective To explore the effects of combining tumor necrosis factor-α (TNF-αt) inhibitor with adenosine A2b receptor antagonist CVT-6883 on asthmatic lung irflammation in mice.Methods A total of 40 female Balb/c mice were evenly randomized into 5 groups,including normal control group,asthma group,CVT-6883 group,CVT-6883 + etanercept group,and etanercept group.The pathological changes in the lungs were determined and the number of white blood cells(WBC) and eosinophil(EOS) in the bronchoalveolar lavage fluid(BALF) was counted by cell count in each group.The levels of TNF-α in BALF were evaluated by enzyme-linked immunosorbent assay (ELISA).The expression of adenosine A2b receptor mRNA in the lung tissues were measured by reverse transcriptionpolymerase chain reaction (RT-PCR).Results 1.The lung tissue in asthma group,dyed by HE,was found to have a large number of airway inflammatory cell infiltration,thickening of the bronchial mucosa,the alveolar septa widened and fracture.In the CVT-6883,CVT-6883 + etanercept and etanercept group,the pathological changes were relieved.2.The WBC and EOS counts in BALF of the asthma group[(413.8 ±5.8)/L,(139.3 ± 1.4)/L] were higher than those of the normal control group [(24.0 ± 1.3)/L,(1.8 ± 0.1)/L,P ＜ 0.05].The WBC and EOS counts of the CVT-6883 group[(111.5 ±3.8)/L,(3.3 ±0.1)/L],the etanercept group + the CVT-6883 group[(173.8 ±3.9)/L,(10.4 ± 0.2)/L],and the etanercept group[(138.4 ± 3.0)/L,(4.1 ± 0.1)/L] were lower than those of the asthma group (P ＜0.05).3.Compared with the control group(100.4 ± 5.7) ng/L,the TNF-α concentration of the asthma group (145.2 ± 8.8) ng/L was significantly higher (P ＜ 0.05) ; the TNF-α concentration of CVT-6883 group (130.9 ± 5.9) ng/L,CVT-6883 + etanercept group(115.7 ± 8.2) ng/L and the etanercept group(122.0 ± 8.7) ng/L,were significantly decreased compared with asthma group (P ＜ 0.05).4.In asthma group (8.9 ± 1.1) compared with the control group(0.6 ± 0.2),the A2bAR (adenosine A2b receptor) mRNA expression was upregulated (P ＜ 0.05) ; CVT-6883 group(1.6 ±0,3),CVT-6883 + etanercept group(2.5 ±0.6) and the etanercept group(5.3 ±0.4),the A2bAR(adenosine A2b receptor) mRNA expression was significantly decreased compared with asthma group (all P ＜0,05).Conclusion Combination of TNF-α inhibitor with adenosine A2b receptor antagonist can reduce asthmatic lung inflammation.

Objective To evaluate the effects of PM2.5 on the differentiation of splenic CD4 + T lymphocytes in acute asthma mice.Methods (1) Mouse models of acute asthma were established by ovalbumin (OVA) sensitization and challenge.(2) PM2.5 was collected in the urban area of Zhanjiang city under heavy traffic and serious air pollution from total suspended particulate(TSP) mid-flow sampler and multistage particles cutters and the dry powder of PM2.5 was prepared.(3) Specific-pathogen free Balb/c mice,female,at 6 to 8 weeks of age were randomly divided into 8 groups (8 mice each group):a negative control group (NC group),asthma control group (AC group),sensitized mice treated with different doses of PM2.5 groups (SP groups) and asthmatic mice treated with different doses of PM2.5 groups (AP groups).SP groups and AP groups were respectively divided into 3 subgroups according to the dose of PM2.5.The AC group,SP groups and AP groups were sensitized on D0,D7 and D14,and the NC group was treated with NS as controls.The SP1/AP1 group,SP2/AP2 group and SP3/AP3 group were respectively given 50 μL PM2.5 suspension.NC group and AC group were instilled with NS as controls.AC group and AP groups were challenged by aerosol of OVA,and NC group and SP group were treated with NS as controls.Twenty-four hours after last challenge,all the mice were sacrificed,and the percentage of regulatory T cells (Treg),T helper cell type 1 (Th1),Th2 and Th17 of splenic CD4 + T lymphocytes was detected by flow cytometry (FCM).Results (1) An OVA-induced mouse models with acute asthma were successfully established.(2) Comparison of the percentage of Treg of splenic CD4 + T lymphocytes:SP group [(12.28 ± 0.73) ％,(11.93 ± 0.81) ％ and (11.70-± 1.14) ％] and AC group [(12.18 ± 1.00) ％] were lower than that in the NC group[(13.50 ± 0.39) ％] (P ＜ 0.05),AP3 group [(10.58 ± 0.65) ％] was lower than that in the AC group and AP1 group [(11.91 ± 0.79) ％] (P ＜ 0.05).(3) Comparison of the ratio of Th1/Th2 of splenic CD4+ T lymphocyte:SP1 group [(7.74 ± 1.21)％] was higher than that in the NC group [(5.52 ± 1.06) ％] (P ＜0.05),SP2 group[(6.30 ±0.58) ％] was lower than that in the SP1 group(P ＜0.05),SP3 group [(4.87 ± 0.82) ％] was lower than that in the SP2 group (P ＜ 0.05);AC group [(3.69-± 0.47) ％] was lower than that in the NC group and SP3 group (P ＜ 0.05);AP3 group [(2.92 ± 0.57) ％] was lower than that in the AC group(P ＜ 0.05).(4) Comparison of the percentage of Th17 of splenic CD4+ T lymphocyte:AP3 group [(1.46 ± 0.39) ％] was higher than that in the NC group [(0.89 ± 0.24) ％] and the AP2 group [(0.83 ± 0.15) ％] (P ＜ 0.001).Conclusions PM2.5 can inhibit splenic CD4 + T lymphocyte of acute asthma mice differentiation into Treg and Th1,and promote their differentiation into Th2 and Th17,through which aggravates inflammation reactions in the airway.

AIM: To study the protective effects of intravenous (iv) CGRP on myocardial injury in rat. METHODS: Establish a rat myocardial ischemic injury model by subcutaneous injection of single dose of isoproterenol (ISO), and treat the model with single dose of iv CGRP. Two hours later, serum CK, LDH, MDA and SOD levels were measured, MDA and SOD in myocardial tissue were tested, and myocardial tissue structures were observed. RESULTS:(1) Serum MDA and tissue MDA levels increased significantly and serum SOD and tissue SOD decreased significantly in injury group, in the CGRP treated group, the above changes were reversed (P