Objective:To prepare the ocular thermosensitive gel of atropine sulfate and study its in vitro release. Methods: The gel formula was optimized by central composite design response surface methodology. The influences of the amounts of poloxamer 407 (P407) and poloxamer 188(P188) on gelling temperature before and after the dilution with simulated tear fluid were investigated. A membraneless dissolution model was used to determine the gel erosion and in vitro release. Results:The optimized gel formula was as follows:23% P407 and 5% P188. The deviations between the measured values and predicted values were all lower than 5%. The in vitro release experiment showed that the gel erosion and the drug release fitted zero-order kinetics equations with promising correlation, indicating a dissolution-controlled release mechanism. Conclusion:The optimization of the ocular thermosensitive gel of atropine sul-fate can be achieved by central composite design response surface methodology with good estimation. The thermosensitive gel with sus-tained drug release property meets the design requirements.

Objective:To study the mechanisms of immune suppression mediated by Gr-1+CDllb+ myeloid derived suppressor cells (Gr-1~+CDllb~+MDSC)from tumor-bearing mice.Methods:Gr-1~+CDllb~+MDSC recruited into spleen and bone marrow of tumor-bearing mice were purified by Percoll,and suppression mediated by MDSC on T cell proliferation from spleen of naive mice was detected by flow cytometry with CSFE and FTTC-anti CD3 staining,and NO,ROS,IL-10 and TGF-β in the supematant of MDSC were detected by Griess and ELISA.Results:There were much more Gr-1~+CDllb~+MDSCs in spleen and bone marrow from tumor-bearing mouse than those of naive mouse,and suppression on T cell proliferation mediated by MDSC from tumor beating mouse was significantly increased,and there were much more NO,ROS,IL-10 and TGF-βin the supematant of these MDSC than that from naive mouse.Conclusion:MDSC from tumor-bearing mice secreted hish level of NO,ROS,IL-10 and TGF-βto induce immune suppression,and inhibite the proliferation of T cells.

Background Previous studies have shown that bisphenol A exposure is associated with the risk of hypertension; however, most of them are cross-sectional and the conclusions are not consistent. Objective To evaluate the association between bisphenol A exposure and the incident risk of hypertension. Methods Based on a nested case-control design involving 1990 subjects derived from the Dongfeng-Tongji cohort, a total of 1080 subjects were included in this study after excluding 887 hypertensive cases at baseline and 23 subjects with missing blood pressure data in follow-up visits. Epidemiological information was collected through questionnaire survey, and serum bisphenol A concentration was detected by high performance liquid chromatography tandem mass spectrometry. Logistic regression model was used to analyze the potential association between serum bisphenol A level and the risk of hypertension incidence, and linear regression model was used to analyze the association between serum bisphenol A level and blood pressure changes between baseline and follow-up. Results The average age of the 1 080 participants was (62.03±7.45) years, of which 41.1% were male. During the follow-up period, a total of 477 (44.2%) developed hypertension. The median serum concentration of bisphenol A in the total population was 3.15 μg·L⁻¹, and the baseline bisphenol A concentration in the new case group (3.24 μg·L⁻¹) was higher than that in the control group (2.98 μg·L⁻¹) (P<0.05). After adjustment for selected covariates, the risk of hypertension increased by 12% (OR=1.12, 95%CI: 1.02, 1.22) for each unit increase in naturally log-transformed bisphenol A; the systolic blood pressure and diastolic blood pressure increased by 1.88 (95%CI: 1.08, 2.69) mmHg and 1.14 (95%CI: 0.68, 1.61) mmHg, respectively. Compared with the low bisphenol A tertile group, the risk of hypertension in the middle tertile and high tertile groups increased by 39% (OR=1.39, 95%CI: 1.01, 1.91) and 40% (OR=1.40, 95%CI: 1.02, 1.93) respectively; the systolic blood pressure increased by 5.91 (95%CI: 3.06, 8.76) mmHg and 5.71 (95%CI: 2.82, 8.59) mmHg, and the diastolic blood pressure increased by 3.09 (95%CI: 3.06, 8.59) mmHg and 2.89 (95%CI: 1.22, 4.57) mmHg, respectively (P_trend<0.001). A positive association between serum bisphenol A level and hypertension was found among those who were female, never/former smokers, never/former drinkers, without family history of hypertension, with physical exercise, and with prehypertension at baseline (P_trend<0.05). There was no interaction between selected stratified variables and bisphenol A levels on hypertension (P_interaction>0.05). Conclusion Bisphenol A exposure is positively associated with the risk of hypertension.