Objective To study the distribution of pathogenic spectrum in children with severe community-acquired pneumonia(CAP) and bacteria antibiotic resistance.Methods One hundred and ninety-three children with severe CAP were enrolled from Mar 2011 to Feb 2012.Sputum specimens were collected for bacterial culture and drug sensitive test.Meanwhile mycoplasma pneumonia and chlamydia trachomatis were detected by fluorescent quantitative polymerase enzyme technology.Antigen of virus were detected by immunofluorescence assay.Results A total of 96 cases (49.7％) were bacteria positive in 193 children with severe CAP.The top four bacteria strains were klebsiella pneumoniae,staphylococcus aureus,escherichia coli and streptococcus pneumoniae.Most of gram-negative bacteria were resistant to ampicillin,cefazolin,ceftriaxone,ceftazidime,and compound sulfamethoxazole,but were sensitive to piperacillin/tazobactam,imipenem,ciprofloxacin,levofloxacin,amikacin.Gram-positive bacteria were resistant to penicillin and erythromycin,but sensitive to vancomycin.Fifty-three cases (27.5 ％,53/193) were virus Positive,81.1％ of which were less than 1 year old.Respiratory syncytial virus accounted for the most prevalent pathogen,followed by adenovirus,influenza virus A.Mycoplasma pneumoniae were positive in 4 patients (2.1％,4/193),chlamydia trachomatis were positive in 3 patients (1.6％,3/193).Mixed infection was found in 23 cases (11.9％,23/193).There were 14 cases (7.2％,14/193) with undetected pathogens.Conclusion Bacterium is the major pathogen in children with severe CAP and the virus is the second.The initial antibiotics administration of piperacillin/tazobactam or carbapenem and vancomycin should be chosen for severe bacteria pneumonia.

Objective To investigate the significance of expressions of neutrophil and lymphocyte CD11b in children with severe pneumonia.Methods Expressions of neutrophils and lymphocytes CD11b were measured by flow cytometry in 36 children with severe pneumonia( severe pneumonia group),compared with 35 children with mild pneumonia ( mild pneumonia group) and 30 healthy children ( control group).Results In acute stage,expressions of neutrophil CD11b in severe pneumonia group and mild pneumonia group were (90.67 ± 7.03 ) ％ and ( 84.03 ± 5.08 ) ％,respectively,both of which were higher than that in control group [ ( 69.32 ± 5.72 ) ％ ] ( P ＜ 0.05 ).Furthermore,in acute stage,expression of neutrophils CD11b in severe pneumonia group was higher than that in mild pneumonia group (P ＜ 0.05 ).In recovery stage,expressions of neutrophil CD11b in children with severe pneumonia and mild pneumonia were(72.68 ±2.07 ) ％ and (71.45 ± 3.21 ) ％,respectively,which were both lower than those in acute stage ( P ＜ 0.05 ).In acute stage,expression of lymphocyte CD11b of children with severe pneumonia was ( 13.35 ± 6.52 )％,which was lower than that of mild pneumonia group [ ( 19.19 ± 6.47 ) ％ ] ( P ＜ 0.05 ),however,no significant difference was found between severe pneumonia group and control group [ ( 12.42 ± 6.43 ) ％ ] ( P ＞0.05).In recovery period,there was no significant difference in the expression of lymphocytes CD11b between severe pneumonia group [ ( 13.37 ± 4.88 ) ％ ] and mild pneumonia group [ ( 13.78 ± 4.53 ) ％ ] ( P ＞0.05).Conclusion Expressions of neutrophil and lymphocyte CD11 b participate in the pathogenesis of severe pneumonia.Detection of CD11b expression is helpful to diagnose severe pneumonia and predict the prognosis.

Objective To evaluate the effect of dexmedetomidine on spinal p38 mitogen?activated protein kinase ( p38MAPK) expression during remifentanil?induced hyperalgesia in rats with incisional pain. Methods Forty?eight healthy male Sprague?Dawley rats, aged 6 weeks, weighing 220-250 g, were ran?domly divided into 4 groups ( n= 12 each) using a random number table: control group ( group C) , inci?sion pain group ( group IP ) , incision pain + remifentanil group ( group IP+R ) , and incision pain +remifentanil + dexmedetomidine group ( group IP+R+D) . After successful establishment of the model of in?cisionsal pian, remifentanil 1?0μg∕kg was infused for 4 h via the tail vein in group IP+R; remifentanil 1?0μg∕kg was infused for 4 h via the tail vein, and dexmedetomidine 10μg∕kg was simultaneously infused for 4 h via the jugular vein in group IP+R+D; the equal volume of normal saline was infused for 4 h via the tail and jugular veins in C and IP groups. The mechanical paw withdrawal threshold ( MWT) was measured at 24 h before operation ( T0 ) , and at 4, 6, 24 and 48 h after the end of drug infusion ( T1?4 ) . After meas?urement of MWT at T4 , the expression of p38MAPK was determined using immuno?histochemistry. Results was up?regulated at T4 in IP and IP+R groups ( P<0?05) , and no significant change was found in the MWT and expression of p38MAPK in group IP+R+D (P>0?05). Compared with group IP, the MWT was signifi?cantly decreased at T1?4, and the expression of p38MAPK was up?regulated at T4 in group P+R, and the MWT was significantly increased at T1?4, and the expression of p38MAPK was down?regulated at T4 in group IP+R+D (P<0?05). Compared with group IP+R, the MWT was significantly increased at T1?4, and the expression of p38MAPK was down?regulated at T4 in group IP+R+D ( P<0?05) . Conclusion The mecha?nism by which dexmedetomidine reduces hyperalgesia induced by remifentanil is related to down?regulation of spinal p38MAPK expression in the rats with incisional pain.

ObjectiveTo investigate the establishment of a predictive model for early virologic response in previously untreated chronic hepatitis B (CHB) patients treated with telbivudine, since early virologic response can predict the long-term efficacy of nucleotide analogues. MethodsA total of 135 CHB patients who visited Mengchao Hepatobiliary Hospital of Fujian Medical University from January 2007 to August 2014 were enrolled and treated with telbivudine (600 mg qd) for at least 24 weeks. Follow-up was performed once every 2 weeks, and the patients′ baseline data and data measured during treatment were recorded. The t-test was used for comparison of continuous data between groups, the chi-square test was used for comparison of categorical data between groups, and the Cox proportional hazards regression model was used to analyze the influencing factors for early virologic response and establish the predictive model. ResultsThe patients without a family history of hepatitis B virus (HBV) infection (P=0.000 3) and with high baseline levels of total bilirubin (TBil) (P=0.002 6) and aspartate aminotransferase (AST) (P=0.007 4) and a low HBV DNA load (P=0.002 3) tended to show early virologic response. The predictive model was established based on these variables, and the risk score (R) of CHB patients was calculated. The CHB patients with R＞0.85 were more likely to achieve early virologic response. ConclusionThe model established based on the four variables of family history, baseline TBil level, baseline AST level, and HBV DNA level can well predict early virologic response in previously untreated CHB patients treated with telbivudine.