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Some rare earth elements are occupational and environmental toxicants and can cause organ and systemic damage; therefore, they have attracted global attention. Neodymium oxide (Nd2O3) is a rare earth element that is refined and significantly utilized in China. The long noncoding RNA (lncRNA) H19 is encoded by the H19/IGF2 imprinted gene cluster located on human chromosome 11p15.5. H19 has become a research focus due to its ectopic expression leading to the promotion of fibrosis. However, the mechanisms by which it causes pulmonary fibrosis are elusive. This investigation indicates that biologically active Nd2O3 increases H19, SNIP1, and c-myc, decreases miR-29a-3p, accelerates macrophage M2 polarization, and causes pulmonary fibrosis in mice lung tissues. In macrophage-differentiated THP-1 cells, Nd2O3 (25 μg/ml) enhanced H19, SNIP1, and c-myc, reduced miR-29a-3p, accelerated macrophages M2 polarization, and stimulated fibrogenic cytokine (TGF-β1) secretion. Furthermore, the coculturing of Nd2O3-treated macrophage-differentiated THP-1 cells. And human embryonic lung fibroblast cells activated lung fibroblast, which increases the levels of collagen I, α-SMA, p-Smad2/3, and Smad4, whereas H19 knockdown or miR-29a-3p upregulation in macrophages had opposite effects. Moreover, it was revealed that H19/miR-29a-3p/SNIP1/c-myc regulatory axis is involved in pulmonary fibrosis induced by Nd2O3. Therefore, this study provides new molecular insights into the mechanism of pulmonary fibrosis by Nd2O3. [ABSTRACT FROM AUTHOR]

The occupational and environmental health safety of rare earths has attracted considerable attention. In China, the rare earth neodymium oxide (Nd 2 O 3) is extensively refined and utilized. However, the mechanisms of Nd 2 O 3 -induced lung injury are elusive. In the present study, we found that exposure of mice to Nd 2 O 3 caused an inflammatory reaction and fibrosis in lung tissues, which was in relation to the Nd 2 O 3 -induced higher levels of the lncRNA H19 (H19), tumor necrosis factor receptor 1 (TNFRSF1A), p-p65, and p-IKKβ and lower levels of miR-29a-3p. Further, in mouse monocyte macrophage leukemia cells (RAW264.7), Nd 2 O 3 induced an inflammatory reaction, increases of H19 and TNFRSF1A levels, decreases of miR-29a-3p levels, and activation of the nuclear factor (NF)-κB signaling pathway. Further, we established that miR-29a-3p regulates TNFRSF1A expression. Up-regulation of miR-29a-3p and down-regulation of H19 blocked the Nd 2 O 3 -induced secretion of TNF-α, MIP-1α, and IL-6; the increases of TNFRSF1A levels; and activation of the NF-κB signaling pathway in RAW264.7 cells. Further, in Nd 2 O 3 -treated RAW26.4 cells, H19 inhibited the expression of miR-29a-3p, which targets TNFRSF1A, and activated the NF-κB signaling pathway to enhance the expression of TNF-α, MIP-1α, and IL-6. Moreover, for mice, up-regulation of miR-29a-3p reversed lung tissue inflammation, pulmonary fibrosis, and activation of the NF-κB signaling pathway induced by Nd 2 O 3. In sum, the present investigation shows that H19 via miR-29a-3p is involved in lung inflammation and pulmonary fibrosis induced by Nd 2 O 3 , which is a mechanism for the Nd 2 O 3 -induced lung inflammatory response and pulmonary fibrosis. This information is useful for development of a biomarker of Nd 2 O 3 -induced lung injury. • Exposure to Nd 2 O 3 causes an inflammatory reaction and fibrosis in lung tissue of mice. • Nd 2 O 3 increases H19 and TNFRSF1A levels, decreases miR-29a-3p levels, and activates the NF-κB signaling pathway in RAW264.7 cells and mice. • H19 via miR-29a-3p-regulated TNFRSF1A is involved in Nd 2 O 3 -induced lung inflammation and pulmonary fibrosis. • The study provide a tool for assessing lung injury risk of Nd 2 O 3 and other environmental factors that induce inflammatory response and pulmonary fibrosis-associated lncRNAs. [ABSTRACT FROM AUTHOR]

With the acceleration of urbanization, the heat island effect, as a prominent feature of urban climate, has attracted more attention. Differences in urban landscape patterns have an essential impact on the urban thermal environment. The objective of the study is to examine the impact of urban landscape types and patterns on surface temperature. Taking Zhengzhou City, China, as an example, using Google Earth remote sensing images, an urban landscape type map was created, and landscape indices were calculated. The land surface temperature (LST) of the study area was retrieved by the Landsat-8 thermal infrared band. Correlation analysis indicated that the relationships between urban landscape patterns and the thermal environment were as follows: (i) The scale indices (percentage of landscape (PLAND), largest patch index (LPI), edge density (ED), patch density (PD)) of urban landscape types with cooling effect (water body, riverfront area, park, high-rise building) were significantly negative correlated with mean LST of each partition. (ii) Conversely, there were significant positive correlations between the PLAND and LPI of landscape types with warming effect (block, development land, railway land) and the LST of the partition. (iii) The DIVISION index of the four kinds of landscapes with cooling effect was highly positively correlated with LST, and the DIVISION and SPLIT indices of the three kinds of landscapes with warming effect displayed a remarkable negative relationship with LST. Therefore, under the condition of scale control, integrated distribution of landscape with cooling effect, scattered distribution of landscape with warming effect, and reduced connectivity of landscape with warming effect will contribute to effectively alleviating the formation of urban heat islands. [ABSTRACT FROM AUTHOR]

Some rare earth elements are occupational and environmental toxicants and can cause organ and systemic damage; therefore, they have attracted global attention. Neodymium oxide (Nd2O3) is a rare earth element that is refined and significantly utilized in China. The long noncoding RNA (lncRNA) H19 is encoded by the H19/IGF2 imprinted gene cluster located on human chromosome 11p15.5. H19 has become a research focus due to its ectopic expression leading to the promotion of fibrosis. However, the mechanisms by which it causes pulmonary fibrosis are elusive. This investigation indicates that biologically active Nd2O3 increases H19, SNIP1, and c-myc, decreases miR-29a-3p, accelerates macrophage M2 polarization, and causes pulmonary fibrosis in mice lung tissues. In macrophage-differentiated THP-1 cells, Nd2O3 (25 μg/ml) enhanced H19, SNIP1, and c-myc, reduced miR-29a-3p, accelerated macrophages M2 polarization, and stimulated fibrogenic cytokine (TGF-β1) secretion. Furthermore, the coculturing of Nd2O3-treated macrophage-differentiated THP-1 cells. And human embryonic lung fibroblast cells activated lung fibroblast, which increases the levels of collagen I, α-SMA, p-Smad2/3, and Smad4, whereas H19 knockdown or miR-29a-3p upregulation in macrophages had opposite effects. Moreover, it was revealed that H19/miR-29a-3p/SNIP1/c-myc regulatory axis is involved in pulmonary fibrosis induced by Nd2O3. Therefore, this study provides new molecular insights into the mechanism of pulmonary fibrosis by Nd2O3. [ABSTRACT FROM AUTHOR]