Quantifying the impacts of human mobility restriction on the spread of coronavirus disease 2019: an empirical analysis from 344 cities of China / 中华医学杂志(英文版)

BACKGROUND@#Since the outbreak of coronavirus disease 2019 (COVID-19), human mobility restriction measures have raised controversies, partly because of the inconsistent findings. An empirical study is promptly needed to reliably assess the causal effects of the mobility restriction. The purpose of this study was to quantify the causal effects of human mobility restriction on the spread of COVID-19.@*METHODS@#Our study applied the difference-in-difference (DID) model to assess the declines of population mobility at the city level, and used the log-log regression model to examine the effects of population mobility declines on the disease spread measured by cumulative or new cases of COVID-19 over time after adjusting for confounders.@*RESULTS@#The DID model showed that a continual expansion of the relative declines over time in 2020. After 4 weeks, population mobility declined by -54.81% (interquartile range, -65.50% to -43.56%). The accrued population mobility declines were associated with the significant reduction of cumulative COVID-19 cases throughout 6 weeks (ie, 1% decline of population mobility was associated with 0.72% [95% CI: 0.50%-0.93%] reduction of cumulative cases for 1 week, 1.42% 2 weeks, 1.69% 3 weeks, 1.72% 4 weeks, 1.64% 5 weeks, and 1.52% 6 weeks). The impact on the weekly new cases seemed greater in the first 4 weeks but faded thereafter. The effects on cumulative cases differed by cities of different population sizes, with greater effects seen in larger cities.@*CONCLUSIONS@#Persistent population mobility restrictions are well deserved. Implementation of mobility restrictions in major cities with large population sizes may be even more important.

Inhibitory effects of phenolic glycoside compound xylocontroside D against Aβ1-42 induced neurotoxicity / 中国药学杂志

OBJECTIVE: To investigate the inhibitory effects of phenolic glycoside compound xylocontroside D on neurotoxicity of primary cultured cortical neurons induced by Aβ1-42. METHODS: The primary cortical neurons and microglia cells derived from rat cerebral tissues were used and neurotoxicity were induced by Aβ1-42. Then the thiazolyl blue tetrazolium bromide test (MTT) was applied for detecting cell survivability; cells were incubated with CH3-H2DCF-DA for evaluating cellular endogenous reactive oxygen species (ROS) level by flow cytometry; fluorescent staining of 8-hydroxy-2-deoxyguanosine (8-OH-DG) was applied for identifying the metabolites of ROS based DNA damage; fluorescent imaging was applied for illustrating the activation of microglia cells and the enzyme-linked immunosorbent assay (ELISA) was applied for analysis of pro-inflammatory cytokines, cyclooxygenase-1 (COX-1), cyclooxygen-ase-2(COX-2), interleukin-1beta (IL-1β) and tumor necrosis factor alpha (TNF-α). RESULTS: Xylocontroside D showed significant inhibitory effects on Aβ1-42 induced neurotoxicity, including cell death, cellular endogenous ROS levels and DNA damage caused by ROS reaction. Moreover, this compound could also prevent the activation of microglia, decrease the production or secretion of proinflammatory cytokines that produced by activated microglia, such as COX-1, COX-2, IL-1β and TNF-α. CONCLUSION: Our results indicated that xylocontroside D was able to inhibit the oxidative stress injury and neuroinflammation of primary cultured cortical neurons induced by Aβ1-42.