Objective To study the diagnostic value of heart fat acid binding protein (h‐FABP) in myocardial damage of children with hand‐foot‐mouth disease (HFMD) .Methods From February 2012 to December 2014 ,100 children with HFMD were chosen as study objects .All children study were divided into 2 sub‐groups according to the severity of disease:71 in ordinary HFMD sub‐group ,29 in severe HFMD sub‐group .At the same time ,100 healthy children were chosen as control group .The routine blood test , rate of abnormal electrocardiography ,rate of abnormal cTnI and rate of abnormal h‐FABP were compared among all children .The cTnI and h‐FABP at different time were compared between ordinary HFMD sub‐group and severe HFMD sub‐group .Results The WBC ,RBC and L had significant difference among different groups/sub‐groups(P<0 .05) ,the difference of PLT had no statistical significance(P>0 .05) .In ordinary HFMD sub‐group ,rate of abnormal electrocardiography was 19 .72% (14/71) ,rate of abnormal cTnI was 4 .23% (3/71)and rate of abnormal h‐FABP was16 .39% (10/71);in severe HFMD group ,rate of abnormal electrocardio‐graphy was 72 .41% (21/29) ,rate of abnormal cTnI was 82 .76% (23/29) and rate of abnormal h‐FABP was 82 .96% (23/29);in control group ,rate of abnormal electrocardiography was 1 .00% (1/100) ,rate of abnormal cTnI was 2 .00% (2/100)and rate of ab‐normal h‐FABP was 0 .00% (0/100) ,the difference had statistical significance(P<0 .05) .The cTnI and h‐FABP at different time had significant difference between ordinary HFMD sub‐group and severe HFMD sub‐group(P<0 .05) .Conclusion Heart fat acid binding protein (h‐FABP) can reflect the early myocardial damage in children with hand‐foot‐mouth disease .

Objective: To analyze the genome characteristics of an avian influenza A (H9N2) virus isolated from an 11-month-old infant, and to look for possible sources of infection. Methods: Throat swabs were collected from an infant with influenza-like illness in influenza sentinel surveillance hospitals and isolated for influenza viruses using cells. The isolates were identified for influenza virus types and subtypes by the method of hemagglutination assay, hemagglutination inhibition assay and fluorescence PCR. Whole genome sequencing of the isolated virus was carried out. The genome nucleic acid sequences and the deduced amino acid sequences were analyzed by comparing the phylogenetic trees which were constructed by bioinformatics software. Results: A seasonal un-typed influenza virus was isolated from the infant with influenza like illness. With fluorescent PCR method , it was identified as H9N2 subtype of avian influenza virus and the case was confirmed as a human infected with an avian influenza A(H9N2) virus. Epidemiological studies revealed that the case had no clear history of poultry contact and exposure. Blast analysis shows that eight segments of the viral genome are avian origin, and 97.5%-99.8% homology with that of viruses isolated from the live-poultry markets. The virus belongs to G57 genotype, deduced amino acid sequence analysis shows that the virus has typical low pathogenic avian influenza characteristics. Conclusions Although the case does not have a clear history of contact or exposure to poultry, molecular traceability suggests that possible sources of infection may be still from poultry.