Background: Limited epidemiological literature identi ed the associations between residential greenness and hypertension in low/middle-income countries.Methods: A random sampling strategy was adopted to recruit 39 259 residents, ≥ 18 years, and from 5 counties in central China. Blood pressure was measured based on the protocol of the American Heart Association. Hypertension was de ned according to the 2010 Chinese guidelines for the management of hypertension. The satellite-derived Normalized Difference Vegetation Index (NDVI) and Enhanced Vegetation Index (EVI) were applied to estimate the residential greenness. Mixed logit model and mixed linear model were utilized to explore the relationships of residential greenness with hypertension and blood pressure.Results: High residential greenness was associated with lower odds of hypertension and blood pressure levels. For instance, an interquartile range (IQR) increase in NDVI 500m was linked with lower odds of hypertension (OR = 0.92, 95%CI 0.88 to 0.95), a decrease of -0.88 mm Hg (95%CI -1.17 to -0.58) and -0.64 mm Hg (95%CI -0.82 to -0.46) in SBP and DBP, respectively. The effect of residential greenness was more pronounced in males, smokers, and drinkers.Conclusions: Long-term exposure to residential greenness may reduce the risk of hypertension. More prospective studies are needed to verify the hypothesis.

No abstract

No abstract

Background: Asthma is characterized by airway hyperresponsiveness (AHR), inflammation, and airway remodeling. Airway hyperresponsiveness results from enhanced airway smooth muscle (ASM) contraction potentially under the control of an epithelium-derived relaxing factor (EpDRF). However, relatively rare is known about EpDRF. We aimed to elucidate the role of epithelium-derived stanniocalcin-1 (STC1) on AHR and ASM contraction. Methods: Stanniocalcin-1 levels in the serum of asthmatic patients and healthy volunteers and in bronchoalveolar lavage fluid (BALF) from ovalbumin (OVA)-challenged mice were measured by ELISA. The effects of exogenous STC1 on AHR and on inflammation were examined in mice. IL-13 modulation of STC1 mRNA and protein levels was studied in human bronchial epithelial cell lines (16HBE). The function of STC1 on Ca 2+ influx and ASM contraction was examined ex vivo. Results: Serum STC1 was decreased in asthma (n = 93) compared with healthy volunteers (1071 ± 30.4 vs 1414 ± 75.1 pg/ml, p < 0.0001, n = 23) and correlated with asthma control (p = 0.0270), lung function (FEV1, p = 0.0130), and serum IL-13 levels (p = 0.0009). Treatment of ten asthmatic subjects with inhaled corticosteroids/ long-acting beta2-agonists (ICS/LABA) for 1 year enhanced STC1 expression which correlated with improved asthma control (p = 0.022). STC1 was mainly expressed in bronchial epithelium and intranasal administration of recombinant human STC1 (rhSTC1) reduced AHR and inflammation in mice. IL-13 suppressed STC1 release from 16HBE, whereas rhSTC1 blocked store-operated Ca 2+ entry (SOCE) by suppressing stromal interaction molecule 1 (STIM1) and further inhibited ASM cell contractility by suppressing Ca 2+ -dependent myosin light chain (MLC) phosphorylation.