[A brief introduction of local allergic rhinitis].

Local allergic rhinitis（local allergic rhinitis, LAR） is a newly proposed concept in recent years. It refers to patients with typical allergic rhinitis symptoms but skin prick test (SPT) and serum specificity IgE are negative, while nasal mucosa can produce local specific IgE and allergen provocation test (NAPT) are positive. The rate of clinical misdiagnose is high. The diagnosis mainly relies on typical nasal symptoms, positive NAPT and/or detection of local specific IgE. It needs to be distinguished from allergic rhinitis(AR) and non-allergic rhinitis (NAR). The main mechanism of its onset is the Th2-type allergic inflammatory response mediated by locally produced IgE. Eosinophils and mast cells are also involved in the inflammatory process. The current study considers LAR to be a separate disease from AR. Allergen immunotherapy(AIT) can be used to treat the disease..

[lambda N gene expression regulated by the leader sequence].

It was reported recently that changing the TIR (translational initiation region) of lambda N gene resulted in the increasing expression of lambda N gene and it was regulated at translational level. According to the alignment, the leader sequence of lambda N gene had three parts: a code region for ORF lambda N, the upstream sequence of ORF lambda N and 17 bp of spacer between ORF lambda N and downstream of lambda N gene. ORF lambda N is an open reading frame located at upstream of lambda N gene coding a peptide of 19 amino acids. To study the mechanism of regulation of lambda N gene expression, three serials of plasmids with mutant leader region of lambda N gene were constructed. (1) pMC1403-XT, in which the start codon or the partial code of ORF lambda N was connected with lacZ to obtain the ORF lambda N-lacZ fusion gene and in which the ORF lambda N-lacZ expression was under the control of a strong trp/lac promoter; (2) The ORF lambda N mutants in which the termination codon TAA was introduced into ORF lambda N at different positions by site-directed mutagenesis to preterminate the ORF lambda N on plasmid pMC1403N; (3) Mutants in which a deletion was located at upstream ORF lambda N in the ORF lambda N mutants above. The results obtained from determination of the beta-galactosidase activity in the transformants harboring the different plasmids showed that the ORF lambda N-lacZ expression was suppressed by the ORF lambda N code region and the lambda N expression was increased in both the second and third serials of mutants. At the same time the results from RNA-DNA dot hybridization showed that the lambda N gene expression was regulated at translational level. Therefore it was predicted that the reason of relatively low expression for lambda N gene in pMC1403N was due to the low efficiency of ORF lambda N translation. There are two ways to increase the expression of lambda N gene. One is to preterminate the translation of ORF lambda N at a suitable position to decrease the ORF lambda N effects on downstream lambda N gene translation; the other is to change the upstream sequence of ORF lambda N to improve its translation efficiency.