Progress in clinical detection of Mycoplasma pneumonia / 中国人兽共患病学报

Mycoplasma pneumonia is one of the important pathogens leading to respiratory tract infection.Recently,the incidence of M.pneumoniae infection increased rapidly,which contributes about 30％ of lung disease in children.The early clinical symptoms for M.pneumoniae infection is not typical,which is not sensitive to antibiotics acting on cell walls.Therefore,early laboratory detection of M.pneumoniae is very important for later treatment.Herein,this paper aims to sum up the recent development progress of M.pneumoniae detection.

Progress in clinical detection of Mycoplasma pneumonia / 中国人兽共患病学报

Mycoplasma pneumonia is one of the important pathogens leading to respiratory tract infection.Recently,the incidence of M.pneumoniae infection increased rapidly,which contributes about 30％ of lung disease in children.The early clinical symptoms for M.pneumoniae infection is not typical,which is not sensitive to antibiotics acting on cell walls.Therefore,early laboratory detection of M.pneumoniae is very important for later treatment.Herein,this paper aims to sum up the recent development progress of M.pneumoniae detection.

Molecular genetic analysis for the A3 alleles / 中国实验血液学杂志

To study four A(3) subgroup samples identified by serologic tests, among which two belong to a family, three were A(3) subgroup, one was A(3)B subgroup. All four samples were genotyped by PCR-SSP method, and the nucleotide sequences of Exon 6, Exon 7 and part introns at the ABO locus for these samples were detected by ABI Prism 3100 DNA sequencer. Comparison with the consensus of A101 was performed. The results showed that haplotypes of two A(3) subgroups were common A102 allele and O1-2 allele, and haplotypes of one A(3) subgroup were common A102 allele and rare O(1v)-4 allele. Unexpectedly, a synonymous substitution 838C-->T had been found in A allele of the A(3)B subgroup sample, which predict a Leu280Phe alteration. The results suggested that molecular genetic background of the A(3) phenotypes is polymorphic. Possibly, the missense mutation 838C-->T is the molecular genetic basis of A(3)B subgroup that lead to low activity of the glycosyltransferases.