Velocity of Ultrasonic Waves in Solutions of Electrolytes

List of the genes involved in CVDs according to DisGeNET database. For each gene all the related diseases and the putative EV-MiRNAs targeting it are indicated both as list and as number of occurrences. (PDF 1206 kb

Lung immunohistochemical analysis.

<p>Immunohistochemical analyses of HO-1 expression in lung tissue 24 h after the third intratracheal instillation; the brown color reflects the site and intensity of HO-1 expression. (A): lung of sham mice; in the box, a control of the immunohistochemical reaction specificity, where the primary antibody has been avoided, in a PM10sum instilled mouse; (B): alveolar and peribronchiolar spaces in the lung of a sham mouse; (C, D): alveolar and peribronchiolar spaces in lungs of PM10sum-treated mice. Each figure represents the status evidenced examining 6 sham and 6 PM10sum-treated mice. A bar = 150 µm; B–D bars = 50 µm.</p

Blood/plasma analysis.

<p>Inflammation and coagulation markers have been analysed in blood/plasma of sham and PM10sum-treated mice. (A): table summarizing assays in blood/plasma from sham (n = 6) and PM10sum-treated mice (n = 6), 24 h after the third intratracheal instillation; (B): immunoblotting results in plasma from sham (n = 6) and PM10sum-treated mice (n = 6), 24 h after the third intratracheal instillation. The proteins have been normalized to albumin and each protein in PM10-treated group has been normalized onto respective sham group. All the data are expressed as mean ± s.e. Sham vs. PM10sum-treated:</p>*<p>p<0.05;</p>**<p>p<0.01.</p

Immunoblotting analysis.

<p>Immunoblotting analysis in lung (A), heart (B) and brain (C) parenchyma from sham (n = 6) and PM10sum-treated mice (n = 6), 24 h after the third intratracheal instillation. The proteins have been normalized to β-actin and each protein in PM10-treated group has been normalized onto respective sham group. All the data are expressed as mean ± s.e. Sham vs. PM10sum-treated:</p>*<p>p<0.05.</p

Blood gene expression.

<p>QPCR gene expression analysis in blood from sham (n = 5) and PM10sum-treated mice (n = 5), 24 h after the third intratracheal instillation.</p

Lung histological analysis.

<p>Histology of lung tissue 24 h after the third intratracheal instillation. (A, B): lung parenchyma of sham mice, showing bronchiolar and alveolar epithelia; (C, D): PM10sum-treated lung parenchyma, showing inflammatory cells recruitment and AMs infiltration (arrows) in the connective surrounding terminal bronchioles and proximal alveolar sacs. Each figure represents the status evidenced examining 6 sham and 6 PM10sum-treated mice. A and C bars = 150 µm; B and D bars = 50 µm.</p

Lung gene expression.

<p>QPCR gene expression analysis in lung parenchyma from sham (n = 5) and PM10sum-treated mice (n = 5), 24 h after the third intratracheal instillation. Sham vs. PM10sum-treated:</p>*<p>p<0.05.</p

BALf analysis.

<p>Several markers have been analysed in the BALf of sham and PM10sum-treated mice. (A): table summarizing results of cell counts and biochemical analysis in BALf from sham (n = 6) and PM10sum-treated mice (n = 6), 24 h after the third intratracheal instillation; (B): immunoblotting results in BALf from sham (n = 6) and PM10sum-treated mice (n = 6), 24 h after the third intratracheal instillation; each protein in PM10-treated group has been normalized onto respective sham group. All the data are expressed as mean ± s.e. Sham <i>vs</i> PM10sum-treated:</p>*<p>p<0.05,</p>**<p>p<0.01.</p

BALf, lung, heart, brain and plasma immunoblotings.

<p>Western blottings displaying proteins in BALf (A), lung (B), heart (C), brain (D) and plasma (E) in sham and PM10sum-treated mice, 24 h after the third intratracheal instillation. Reported blots are representative of 6 sham and 6 PM10sum-treated mice; densitometry analyses are reported in Tab.1.</p

Health Risk Assessment for Air Pollutants: Alterations in Lung and Cardiac Gene Expression in Mice Exposed to Milano Winter Fine Particulate Matter (PM2.5)

<div><p>Oxidative stress, pulmonary and systemic inflammation, endothelial cell dysfunction, atherosclerosis and cardiac autonomic dysfunction have been linked to urban particulate matter exposure. The chemical composition of airborne pollutants in Milano is similar to those of other European cities though with a higher PM2.5 fraction. Milano winter fine particles (PM2.5win) are characterized by the presence of nitrate, organic carbon fraction, with high amount of polycyclic aromatic hydrocarbons and elements such as Pb, Al, Zn, V, Fe, Cr and others, with a negligible endotoxin presence. In BALB/c mice, we examined, at biochemical and transcriptomic levels, the adverse effects of repeated Milano PM2.5win exposure in lung and heart. We found that ET-1, Hsp70, Cyp1A1, Cyp1B1 and Hsp-70, HO-1, MPO respectively increased within lung and heart of PM2.5win-treated mice. The PM2.5win exposure had a strong impact on global gene expression of heart tissue (181 up-regulated and 178 down-regulated genes) but a lesser impact on lung tissue (14 up-regulated genes and 43 down-regulated genes). Focusing on modulated genes, in lung we found two- to three-fold changes of those genes related to polycyclic aromatic hydrocarbons exposure and calcium signalling. Within heart the most striking aspect is the twofold to threefold increase in collagen and laminin related genes as well as in genes involved in calcium signaling. The current study extends our previous findings, showing that repeated instillations of PM2.5win trigger systemic adverse effects. PM2.5win thus likely poses an acute threat primarily to susceptible people, such as the elderly and those with unrecognized coronary artery or structural heart disease. The study of genomic responses will improve understanding of disease mechanisms and enable future clinical testing of interventions against the toxic effects of air pollutant.</p></div