The relevance analysis methods for the association between environmental factors (air pollutants, fine particles, climate conditions, toxic materials) and diseases (lung cancer and asthma, etc) were studied by mining the open access scientific data in American environmental health field, which realized their practical application and can thus provide reference for studying the association between environments and diseases in our country.

A model of classification techniques was established according to the sex and age by quantitative analy-sis of the risk factors for air popplution-induced respiratory diseases using the C4 .5 decision-making tree classifi-cation.The classification-based quantitative analysis was studied.The role of risk factors for respiratory diseases in 9 groups of people was assayed .This method can be used to analyze the risk factors for both respiratory diseases and other diseases in different populations, and can thus provide the evidence for their prevention and control.

Objective To explore the relationship of the expression, regulation and adhesion of PTA1 in pregnancy induced hypertension(PIH). Methods The expression,regulation and adhesion of PTA1 on vascular en- dothelial cells incubated by sera from 10 PIH patients and 10 normal pregnant women repectively was detected by flow cytometry. Results The positive rate of PTA1 15.51% (24h) and 6.32 % (48h) in PIH group is significantly higher than that 7.81% (24h) and 4.72 % (48h) in normal pregnant woman group( P < 0.01 ). After the incubation with platelets,the positive rate of PTA1 6.64% (24h) and 4.13% (48h) in PIH group is lower than before(P< 0.05). The PTA1 expression 8.11% (24h) and 4.28% (48h) in PIH group is much lower after blocking with PTA1/IgG than that before(P < 0.01 ). Conclusion There are some abnormal stimulated factors in PIH patients, which activate vascular endothelial cells. PTA1 plays an important role in the adhesion of platelets to vascular en- dothelial cells, PTA1 is closely related to the progress of PIH which indicates that PTA1 directly or indirectly takes part in the pathophysiologic consequences of PIH.