公共危机情境下“柔性治理”如何跨越“数字鸿沟”?——基于三种政策工具的实证研究

在近年来发生的公共危机治理过程中,数字治理技术发挥着重要的作用,但在社区推广层面面临着“数字鸿沟”的现实难题。作为基层社区的重要政策工具,“柔性治理”如何帮助社区民众跨越“数字鸿沟”?在行为公共管理视角下,论文选取健康码的社区推广过程为研究背景,采用双因素(2×3)被试间设计开展调查实验(N=436),以“数字治理民众支持度”为被解释变量,重点探究“数字鸿沟”情景下三种“柔性治理”政策工具的选择策略,并以社区老人、社工访谈为实验结论佐证。实证结果显示,“数字鸿沟”情景对数字治理民众支持度起显著消解作用;三种“柔性治理”政策工具的主效应对被解释变量的影响无显著差异,但“数字鸿沟”情景中的激励工具和助推工具更起显著提升作用。研究用实证分析打开了“柔性治理”政策工具作用机制的“黑箱”,一方面启示管理者应兼顾目标群体特征、政策工具特征和“数字鸿沟”情景,精准施策推动社区数字治理高质量发展;另一方面强调“工具-情景”匹配的政策评估范式,推动行为公共政策在应急管理中向纵深化发展。

The role of endothelial biomarkers in predicting damp-heat syndrome in diabetic kidney disease

Objective:To explore the role of endothelial biomarkers in predicting damp-heat syndrome in diabetic kidney disease(DKD).Methods:A total of 183 patients with DKD were divided into 3 groups:the early DKD group,established DKD group,and advanced DKD group.All patients were classified according to traditional Chinese medicine(TCM)syndrome type,and clinical indexes were collected for statistical analysis.Results:A total of 183 DKD patients were included in this study.Fibroblast growth factor 23(FGF23),chitinase-3-like protein 1(CHI3L1),endocan,tumor necrosis factor receptor 1(TNFR1),secretory leukocyte protease inhibitor(SLPI),and vascular endothelial growth factor A(VEGF-A)were increased in advanced DKD.FGF23,CHI3L1,endocan,SLPI,and TNFR1 showed a negative correlation with estimated glomerular filtration rate(eGFR),while they had a positive correlation with 24 h urine protein.After adjusting for age,gender,diabetes duration,body mass index(BMI),hemoglobin,glucose,uric acid,24 h urine protein,cholesterol,triglyceride,low-density lipoprotein,and hemoglobin A1c(HbA1c),the multiple regression analysis showed that FGF23,endocan,TNFR1,and SLPI significantly correlated with eGFR.Conclusions:FGF23,endocan,TNFR1,and SLPI are elevated in advanced DKD compared with early stage,and they may take part in the pathogenesis and progression of DKD.Our study provides useful biomarkers for predicting the appearance of damp-heat syndrome,including FGF23,endocan,TNFR1,and SLPI.

Human mesenchymal stromal cells enhance the immunomodulatory function of CD8＋CD28- regulatory T cells

One important aspect of mesenchymal stromal cells （MSCs）-mediated immunomodulation is the recruitment and induction of regulatory T （Treg） cells. However, we do not yet know whether MSCs have similar effects on the other subsets of Treg cells. Herein, we studied the effects of MSCs on CD8＋CD28- Treg cells and found that the MSCs could not only increase the proportion of CD8＋CD28- T cells, but also enhance CD8＋CD28-T cells＇ ability of hampering naive CD4＋ T-cell proliferation and activation, decreasing the production of IFN-γ by activated CD4＋ T cells and inducing the apoptosis of activated CD4＋ T cells. Mechanistically, the MSCs affected the functions of the CD8＋CD28- T cells partially through moderate upregulating the expression of IL-10 and FasL. The MSCs had no distinct effect on the shift from CD8＋CD28＋ T cells to CD8＋CD28- T cells, but did increase the proportion of CD8＋CD28- T cells by reducing their rate of apoptosis. In summary, this study shows that MSCs can enhance the regulatory function of CD8＋CD28- Treg cells, shedding new light on MSCs-mediated immune regulation.

Mesenchymal stromal cells alleviate acute respiratory distress syndrome through the cholinergic anti-inflammatory pathway

Mesenchymal stromal cells(MSCs)have been considered a promising alternative for treatment of acute respiratory distress syndrome(ARDS).However,there is significant heterogeneity in their therapeutic efficacy,largely owing to the incomplete understanding of the mechanisms underlying the therapeutic activities of MSCs.Here,we hypothesize that the cholinergic antiinflammatory pathway(CAP),which is recognized as a neuroimmunological pathway,may be involved in the therapeutic mechanisms by which MSCs mitigate ARDS.Using lipopolysaccharide(LPS)and bacterial lung inflammation models,we found that inflammatory cell infiltration and Evans blue leakage were reduced and that the expression levels of choline acetyltransferase(ChAT)and vesicular acetylcholine transporter(VAChT)in lung tissue were significantly increased 6 hours after MSC infusion.When the vagus nerve was blocked orα7 nicotinic acetylcholine(ACh)receptor(α7nAChR)-knockout mice were used,the therapeutic effects of MSCs were significantly reduced,suggesting that the CAP may play an important role in the effects of MSCs in ARDS treatment.Our results further showed that MSC-derived prostaglandin E2(PGE2)likely promoted ACh synthesis and release.Additionally,based on the efficacy of nAChR andα7nAChR agonists,we found that lobeline,the nicotinic cholinergic receptor excitation stimulant,may attenuate pulmonary inflammation and alleviate respiratory symptoms of ARDS patients in a clinical study(ChiCTR2100047403).In summary,we reveal a previously unrecognized MSC-mediated mechanism of CAP activation as the means by which MSCs alleviate ARDS-like syndrome,providing insight into the clinical translation of MSCs or CAP-related strategies for the treatment of patients with ARDS.

含呋喃环生物基聚酰胺的合成

随着环境保护和化石资源问题的日益严峻,开发基于可再生生物质资源的生物基高分子材料,成为未来的发展趋势。作为最具有价值的生物基平台化合物之一,呋喃二甲酸及其衍生物可用于制造精细化学品和高分子材料。近年来,通过熔融聚合、溶液聚合、界面缩聚和固相缩聚等方法,将呋喃二甲酸及其衍生物与二元胺反应,制备出不同结构的生物基聚酰胺的均聚物和共聚物。本文从单体、聚合方法、聚合物结构和性能等方面,对含呋喃环生物基聚酰胺的合成作一总结,同时对这一领域的前景和挑战进行了探讨。