Characteristics of the studies included in the meta-analysis.

<p>*This number indicates the total number of CAS and CEA procedures performed in each study and for which the DWI is available.</p><p>**The reported characteristics refer to the overall population included in the original study and not to the 58 included in the meta-analysis because of DWI availability.</p><p>Abbreviations: CAD = coronary artery disease; CAS = carotid artery stenting; CEA = carotid endarterectomy; EPD = embolic protection device; ICSS-MRI = international carotid stenting study-magnetic resonance imaging; RCT = randomized clinical trial</p><p>Characteristics of the studies included in the meta-analysis.</p

Post-procedural stroke after CAS and CEA.

<p>Random effects odds ratio and 95% confidence interval for the post-procedural incidence of stroke after CAS and CEA.</p

New DWI cerebral lesions after CAS and CEA.

<p>Random effects odds ratio and 95% confidence interval for the primary endpoint of new ischemic lesions at DWI after CAS and CEA.</p

Flow diagram.

<p>Studies included in the meta-analysis.</p

Improved Time-Resolved Measurements of Inorganic Ions in Particulate Matter by PILS-IC Integrated with a Sample Pre-Concentration System

<div><p>A particle-into-liquid sampler coupled with ion chromatograph (PILS-IC) for the on-line measurement of inorganic ions has been modified by the insertion of two ion-exchange pre-concentration cartridges that enrich the sample during the period of the IC analysis. The limits of detection of the modified instrument were 10-15 times lower and the time coverage 24 times higher (from 2 to 48 min per hour) than those of the original PILS-IC setup. The instrumental performance in terms of recovery and break-through volume from the cartridges was satisfactory. The modified PILS-IC was operated in comparison with a diffusion denuder line and with a high-resolution time-of-flight aerosol mass spectrometer (HR-TOF-AMS) during a short intensive measurement period organized in the framework of the European Monitoring and Evaluation Programme (EMEP), a co-operative program for monitoring and evaluation of the long-range transmission of the air pollutants in Europe. The instrument showed a quantitative response in agreement with the results of the diffusion lines, and an ability to trace fine concentration variations not so different from the performance of the much more complex HR-TOF-AMS. From the time patterns of the ion concentrations measured by the modified PILS-IC, it was possible to obtain useful information about the variations in the air quality and in the strength of the particulate matter sources.</p><p>Copyright 2015 American Association for Aerosol Research</p></div

Epigenetic Switch at Atp2a2 and Myh7 Gene Promoters in Pressure Overload-Induced Heart Failure

<div><p>Re-induction of fetal genes and/or re-expression of postnatal genes represent hallmarks of pathological cardiac remodeling, and are considered important in the progression of the normal heart towards heart failure (HF). Whether epigenetic modifications are involved in these processes is currently under investigation. Here we hypothesized that histone chromatin modifications may underlie changes in the gene expression program during pressure overload-induced HF. We evaluated chromatin marks at the promoter regions of the sarcoplasmic reticulum Ca²⁺ATPase (SERCA-2A) and β-myosin-heavy chain (β-MHC) genes (Atp2a2 and Myh7, respectively) in murine hearts after one or eight weeks of pressure overload induced by transverse aortic constriction (TAC). As expected, all TAC hearts displayed a significant reduction in SERCA-2A and a significant induction of β-MHC mRNA levels. Interestingly, opposite histone H3 modifications were identified in the promoter regions of these genes after TAC, including H3 dimethylation (me2) at lysine (K) 4 (H3K4me2) and K9 (H3K9me2), H3 trimethylation (me3) at K27 (H3K27me3) and dimethylation (me2) at K36 (H3K36me2). Consistently, a significant reduction of lysine-specific demethylase KDM2A could be found after eight weeks of TAC at the Atp2a2 promoter. Moreover, opposite changes in the recruitment of DNA methylation machinery components (DNA methyltransferases DNMT1 and DNMT3b, and methyl CpG binding protein 2 MeCp2) were found at the Atp2a2 or Myh7 promoters after TAC. Taken together, these results suggest that epigenetic modifications may underlie gene expression reprogramming in the adult murine heart under conditions of pressure overload, and might be involved in the progression of the normal heart towards HF.</p></div

Recruitment of KDM2A and anti-dimethyl-H3K36 (H3K36me2) at Atp2a2 and Myh7 gene promoter regions in TAC hearts.

<p>ChIP experiments were performed using antibodies indicated in each panel: <b>A</b> KDM2A; <b>B–C</b> anti-dimethyl-H3K36 (H3K36me2). Each experiment was repeated at least three times, and the quantitative PCR analyses were performed in triplicate. The data are presented as percentages (%) of input DNA (mean ± SD; *p<0.05 vs. SHAM; **p<0.01 vs. SHAM; n = 4–6 hearts/group).</p

Chromatin modifications at the Atp2a2 and Myh7 gene promoters in murine heart failure.

<p>ChIP experiments were performed at the Atp2a2 or Myh7 gene promoters using anti-dimethyl-H3K4 (H3K4me2; <b>A</b> and <b>B</b>), anti-dimethyl-H3K9 (H3K9me2; <b>C</b> and <b>D</b>) and anti-trimethyl-H3K27 (H3K27me3; <b>E</b> and <b>F</b>) antibodies. Each experiment was repeated at least three times, and the quantitative PCR analyses were performed in triplicate. The data are presented as percentages (%) of input DNA (mean ± SD; *p<0.05 vs. SHAM; **p<0.01 vs. SHAM; n = 4–6 hearts/group).</p

Molecular events underlying the epigenetic switch of the Atp2a2 gene promoter in murine heart failure.

<p>Activating chromatin modifiers and modifications are reported in green, while repressive marks are shown in red. DNA methyl-binding proteins are yellow.</p

Atp2a2 and Myh7 promoter modifications in pressure overload-induced heart failure.

<p>ChIP experiments were performed using antibodies indicated in each panel: <b>A,C</b> anti-DNMT1; <b>B,D</b> anti-DNMT3b; <b>E–F</b> anti-MeCp2. Each experiment was repeated at least three times, and the quantitative PCR analyses were performed in triplicate. The data are presented as percentages (%) of input DNA (mean ± SD; *p<0.05 vs. SHAM; **p<0.01 vs. SHAM; n = 4–6 hearts/group).</p