Objective To investigate the levels of creatine kinase (CK-MB), brain natriuretic peptide (BNP), and neu-ropeptide Y (NPY) in severe pneumonia pediatric patients combined with heart failure (HF). Methods Pneumonia pediatric patients admitted from December 2010 to December 2014 had been enrolled and divided into pneumonia group (P) (n=32), se-vere pneumonia group (SP) (n=20) and severe pneumonia combined HF group (HF) (n=36). Twenty healthy children served as control group (C). Serum level of CK-MB was detected by enzyme rate method and were measured by ELISA. BNP and NPY were measured again during the recovery period in 18 cases in HF group. Results The serum levels of CK-MB, BNP and NPY were signiifcantly different among the four groups, (F=25.19~277.94, P<0.01). The serum levels of CK-MB, BNP and NPY were signiifcantly higher in HF group than in SP, P and C group (P<0.05). The serum level of CK-MB was signiifcantly higher in SP group than that in P and C group (P<0.05) and there was no difference between P and C group (P>0.05). The serum levels of BNP and NPY were not statistically signiifcant between SP and P and C group (all P>0.05). In HF group, the serum levels of CK-MB, BNP, and NPY were signiifcantly decreased in 18 cases after treatment. The serum level of BNP was positively correlat-ed with CK-MB and NPY (r=0.681, 0.525, all P<0.01) and the NPY and CK-MB levels were also positively correlated (r=0.545, P<0.01). Conclusions The Detection of the serum levels of CK-MB, BNP and NPY can help diagnose severe pneumonia com-bined with HF. The BNP maybe the most sensitive indicator.

Objective To investigate the single nucleotide polymorphisms ( SNP) of IL-13G+2044A and IL-13A-1512C and to analyze their relationships with the occurrence of bronchial asthma in chil-dren in Guiyang city. Methods Sequenom MassArray platform, a newly developed genotyping assay, was used to detect the G+2044A locus and the A-1512C locus in 153 subjects with asthma and 103 healthy sub-jects. Then the results were statistically analyzed with chi-square test and t-test. Results Three genotypes of IL-13G+2044A locus including GG, GA and AA were detected in the subjects with or without asthma. There were significant differences in the genotype distribution between the subjects with or without asthma (χ2 =7. 691, P<0. 05). The subjects carrying the variant allele A at IL-13G+2044A locus were more likely to have asthma than those not harboring the variant allele A. There were significant differences in allele fre-quency between the subjects with or without asthma (χ2 = 7. 458, P<0. 01). Three genotypes of IL-13A-1512C locus including AA, AC and CC were detected in the subjects from both of the two groups. There were significant differences in the genotype distribution between the two groups (χ2 = 12. 906, P<0. 01). The variant allele C at IL-13A-1512C locus was associated with lower risk for asthma. Significant differences in allele frequency were observed the two groups (χ2 =10. 407, P<0. 01). Conclusion Both of the alleles at IL-13G+2044A and IL-13A-1512C loci were associated with asthma. The variant allele A at IL-13G+2044A locus might be the gene predisposing children to asthma in Guiyang city. Children carrying the variant allele C at IL-13A-1512C locus showed a lower risk for asthma in Guiyang city.

Orthodontic tooth movement elicits alveolar bone remodeling and orofacial pain that is manifested by tooth mechanical hyperalgesia. Nerve growth factor (NGF) is upregulated in periodontium and may modulate tooth mechanical hyperalgesia. The objectives were to examine the role of NGF in tooth mechanical hyperalgesia and to elucidate the underlying mechanisms. Tooth mechanical hyperalgesia was induced by ligating closed coil springs between incisors and molars in Sprague-Dawley rats. Retrograde labeling was performed by periodontal administration of fluor-conjugated NGF and the detection of fluorescence in trigeminal ganglia (TG). Lentivirus vectors carrying NGF shRNA were employed to knockdown the expression of NGF in TG. The administration of agonists, antagonists, and virus vectors into TG and periodontium was conducted. Tooth mechanical hyperalgesia was examined through the threshold of biting withdrawal. Our results revealed that tooth movement elicited tooth mechanical hyperalgesia that could be alleviated by NGF neutralizing antibody and that NGF was upregulated in periodontium (mainly in periodontal fibroblasts) and TG. Retrograde labeling revealed that periodontal NGF was retrogradely transported to TG after day 1. Acid-sensing ion channel 3 (ASIC3) and NGF were co-expressed in trigeminal neurons and the percentage of co-expression was significantly higher following tooth movement. The administration of NGF and NGF neutralizing antibody into TG could upregulate and downregulate the expression of ASIC3 in TG, respectively. NGF aggravated tooth mechanical hyperalgesia that could be alleviated by ASIC3 antagonist (APETx2). Moreover, NGF neutralizing antibody mitigated tooth mechanical hyperalgesia that could be recapitulated by ASIC3 agonist (GMQ). NGF-based gene therapy abolished tooth mechanical hyperalgesia and downregulated ASIC3 expression. Taken together, in response to force stimuli, periodontal fibroblasts upregulated the expressions of NGF that was retrogradely transported to TG, where NGF elicited tooth mechanical hyperalgesia through upregulating ASIC3. NGF-based gene therapy is a viable method in alleviating tooth-movement-induced mechanical hyperalgesia.