[Time-series analysis on the relationship between ambient PM2.5 and daily outpatient visits due to allergic conjunctivitis among children in Shenzhen].

Objective: To explore the short-term effects of ambient PM2.5 on the outpatient visits of allergic conjunctivitis among children in Shenzhen. Methods: It was a ecological study. Data on daily visits including date of visit, sex and age from children with allergic conjunctivitis were collected from Shenzhen Eye Hospital and Shenzhen Children's Hospital in 2018. Related data on air pollution (PM2.5, PM10, SO2, NO2, CO and O3) and meteorology (atmospheric pressure, temperature and relative humidity) were also collected. Pearson correlation analysis was used for normal distribution data and Spearman rank correlation analysis was used for non-normal distribution data. Generalized additive model was used to estimate the impact of PM2.5 pollution on allergic conjunctivitis outpatients and the lagging effects. Results: In 2018, there were 16 133 allergic conjunctivitis outpatients in the two hospitals. The maximum age was 18 years and the minimum age was 2 months. Males accounted for 49.3%. The daily average concentration of PM2.5 was 22 (15, 31) µg/m3. Changes of the concentration of PM2.5 had a positive correlation with the amount of allergic conjunctivitis visits, and the Spearman correlation coefficient was 0.150 (P=0.004). The single pollutant model showed that the strongest effect appeared at 3 days (RR=1.111， 95%CI:1.071-1.152). A 10 µg/m3 increase of PM2.5 would result in an excessive number of allergic conjunctivitis outpatients as much as 11.112% (95%CI：7.011%-15.212%). In the multiple air pollutants models, after the introduction of NO2, O3 and CO, the concentration of PM2.5 showed an enhanced effect on the number of hospital visits due to allergic conjunctivitis on the same day, and the difference was statistically significant (P<0.05). Conclusion: Changes of the concentration of PM2.5 had a positive correlation with daily outpatient visits of allergic conjunctivitis among children in Shenzhen. (Chin J Ophthalmol, 2020, 56: 608-614).

Piperbetol, methylpiperbetol, piperol A and piperol B: a new series of highly specific PAF receptor antagonists from Piper betle.

Piperbetol, methylpiperbetol, piperol A, and piperol B, isolated from Piper betle, selectively inhibited the washed rabbit platelet aggregation induced by platelet activating factor (PAF) in a concentration-dependent manner. The IC50 values of piperbetol, methylpiperbetol, piperol A, piperol B, and ginkgolide B were about 18.2, 10.6, 114.2, 11.8, and 4.8 mumol/l, respectively. The inhibitory potency of ginkgolide B was about 2.8, 1.2, 22.8, and 1.4 times higher than those of piperbetol, methylpiperbetol, piperol A, and piperol B. The concentration-response curve of PAF-induced platelet aggregation was shifted to the right by 50 mumol/l of piperbetol, methylpiperbetol, piperol A, piperol B, and ginkgolide B. The EC50 of PAF was increased by these compounds from 1.5 nmol/l to 14.3, 23.1, 2.4, 20.6, and 47.2 nmol/l, respectively. The compounds also inhibited the binding of [3H]-PAF to washed rabbit platelets with IC50 values of 8.7, 5.3, 88, 6.2, and 1.8 mumol/l. Correlating with the inhibitory potency for platelet aggregation, the inhibitory potency of ginkgolide B for binding of PAF was about 3.8, 1.9, 48, and 2.4 times higher than those of piperbetol, methylpiperbetol, piperol A, and piperol B. However, the aggregation of washed rabbit platelets induced by threshold ADP and arachidonic acid were unaffected by piperbetol, methylpiperbetol, piperol A, and piperol B. Furthermore, piperbetol, methylpiperbetol, piperol A, and piperol B had no effects on the cAMP contents in rest washed rabbit platelets. In conclusion, these data indicate that piperbetol, methylpiperbetol, piperol A, and piperol B are effective PAF receptor antagonists in vitro.

Effects of CI-930, a novel phosphodiesterase III inhibitor, on platelet aggregation and arachidonic acid metabolism.

In the platelet-rich plasma of rabbits, 4,5-dihydro-6-[4-(1H-imidazol-1-yl)phenyl]-5-methyl-3(2H)-pyridazinone (CI-930) inhibited platelet aggregation triggered by AA, U-46619, ADP, collagen and PAF, with the IC50 values of 0.91, 0.73, 2.12, 2.35 and 7.15 mumols/L, respectively. The inhibitory effect of CI-930 on AA-induced aggregation was potentiated by PGE1, an adenylate cyclase activator, and antagonized by SQ-22536, an adenylate cyclase inhibitor. The contents of cAMP in washed rabbit platelets were increased by CI-930 5-50 mumols/L. In the concentration range of 0.5-500 mumols/L, CI-930 reduced the synthesis of TXB2 by either washed rat or rabbit platelets or rat pleural neutrophils. At the same time, CI-930 induced a dose-dependent increase of PGE2, PGF2a, and PGD2 biosynthesis by rat platelets and had no significant influence on the formation of 6-keto-PGF1a by the neutrophils. It is showed that CI-930 is an anti-platelet agent with a wide-spectrum activity and its anti-aggregating action may be exerted by dual mechanisms, both increasing cAMP contents and selectively inhibiting TXA2 synthesis in platelets.