Objective To investigate the distribution,epidemiologic feature and the related risk features of allergic rhinitis among college students in Kunming.Methods Stratified cluster sampling was conducted in each school as a unit.The investigated subjects included 1500 students aged from18 to 29 years old from 7 universities in Kunming,Yunnan Province.The epidemiological investigation was carried out using the designed questionnaire of allergic rhinitis.The results were analyzed.Restlts We had given out 1500 questionnaires and the response rate was 98.9％.The self-reported prevalence of allergic rhinitis was 25.4％ among college students in Kunming,in which,the males' prevalence rate was 29.3％ and the females' was 22.9％.And 3.7％ of the students with allergic rhinitis were combined with asthma and the 19.1％ combined with a history of familial inheritance.The main risk factor was dust.Concltsion The self-reported and prevalence of allergic rhinitis among college students in Kunming is 25.4％.Males' prevalence rate is slightly higher than the females'.The potential risk factors are bronchial asthma and the history of familial inheritance.The mainly inducement is dust,animal fur and plant pollen.

Objective:To investigate the expressions and significance of tyrosine kinase receptor EphA2 and its ligand ephrinA1 in human malignant gliomas and their correlation with tumor angiogenesis. Methods:The expressions of EphA2, ephrinA1, and CD105-stained microvessel density (MVD) were detected via immunohistochemical assay in 62 glioma tissues and 8 normal brain tissues. The correlation between EphA2 and ephrinA1 expression and microvessel counts in the glioma tissues were assessed. Results:Immunohistochemical staining results revealed that variable levels of EphA2 and MVD expression were significantly higher than that of the normal brain samples. Statistical difference was observed in EphA2 and MVD expressions between human gliomas and normal brain samples (P<0.01). The positive rate of EphA2 and MVD expressions was significantly higher in high-grade gliomas (WHO III-IV) than that in low-grade gliomas (WHO I-II) (P<0.01). EphrinA1 was expressed at low levels in most malignant gliomas, and the increased ephrinA1 expression was associated with lower-grade histology. MVD was significantly positively correlated with EphA2 expression (r=0.713, P<0.01) and significantly negatively correlated with ephrinA1 expression (r=-0. 772, P<0.01). EphA2 was significantly negatively correlated with ephrinA1 expression (r=-0.912, P<0.01). Conclusion:Specifically over-expressed EphA2 and its low-expressed ligand ephrinA1 in malignant gliomas may be closely correlated with the invasion and malignant degree of gliomas. Cooperation is involved in the angiogenesis and has an important function in the initiation and progression of gliomas.

In the original publication, the label of Fig. 2C should be read as "GFAP/lectin/DAPI" not "DMP1/GFAP/lectin/DAPI".

The blood-brain barrier (BBB) is a tight boundary formed between endothelial cells and astrocytes, which separates and protects brain from most pathogens as well as neural toxins in circulation. However, detailed molecular players involved in formation of BBB are not completely known. Dentin matrix protein 1 (DMP1)-proteoglycan (PG), which is known to be involved in mineralization of bones and dentin, is also expressed in soft tissues including brain with unknown functions. In the present study, we reported that DMP1-PG was expressed in brain astrocytes and enriched in BBB units. The only glycosylation site of DMP1 is serine89 (S89) in the N-terminal domain of the protein in mouse. Mutant mice with DMP1 point mutations changing S89 to glycine (S89G), which completely eradicated glycosylation of the protein, demonstrated severe BBB disruption. Another breed of DMP1 mutant mice, which lacked the C-terminal domain of DMP1, manifested normal BBB function. The polarity of S89G-DMP1 astrocytes was disrupted and cell-cell adhesion was loosened. Through a battery of analyses, we found that DMP1 glycosylation was critically required for astrocyte maturation both in vitro and in vivo. S89G-DMP1 mutant astrocytes failed to express aquaporin 4 and had reduced laminin and ZO1 expression, which resulted in disruption of BBB. Interestingly, overexpression of wild-type DMP1-PG in mouse brain driven by the nestin promoter elevated laminin and ZO1 expression beyond wild type levels and could effectively resisted intravenous mannitol-induced BBB reversible opening. Taken together, our study not only revealed a novel element, i.e., DMP1-PG, that regulated BBB formation, but also assigned a new function to DMP1-PG.
Animals ; Astrocytes ; cytology ; metabolism ; Blood-Brain Barrier ; cytology ; metabolism ; Cells, Cultured ; Extracellular Matrix Proteins ; genetics ; metabolism ; Female ; Glycosylation ; Male ; Mice ; Proteoglycans ; metabolism ; Reverse Transcriptase Polymerase Chain Reaction