Discovery of chimeric RNAs, which are produced by chromosomal translocations as well as the joining of exons from different genes by trans-splicing, has added a new level of complexity to our study and understanding of the transcriptome. The enhanced ChiTaRS-3.1 database (http://chitars.md.biu.ac.il) is designed to make widely accessible a wealth of mined data on chimeric RNAs, with easy-to-use analytical tools built-in. The database comprises 34 922 chimeric transcripts along with 11 714 cancer breakpoints. In this latest version, we have included multiple cross-references to GeneCards, iHop, PubMed, NCBI, Ensembl, OMIM, RefSeq and the Mitelman collection for every entry in the ‘Full Collection’. In addition, for every chimera, we have added a predicted chimeric protein–protein interaction (ChiPPI) network, which allows for easy visualization of protein partners of both parental and fusion proteins for all human chimeras. The database contains a comprehensive annotation for 34 922 chimeric transcripts from eight organisms, and includes the manual annotation of 200 sense-antiSense (SaS) chimeras. The current improvements in the content and functionality to the ChiTaRS database make it a central resource for the study of chimeric transcripts and fusion proteins.

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-specific strain analysis: investigation of regional deformations in a rat model of acute versus chronic myocardial infarction. Am J Physiol Heart Circ Physiol 303: H549 -H558, 2012. First published July 9, 2012; doi:10.1152/ajpheart.00294.2012.-Myocardial infarction (MI) injury extends from the endocardium toward the epicardium. This phenomenon should be taken into consideration in the detection of MI. To study the extent of damage at different stages of MI, we hypothesized that measurement of layer-specific strain will allow better delineation of the MI extent than total wall thickness strain at acute stages but not at chronic stages, when fibrosis and remodeling have already occurred. After baseline echocardiography scans had been obtained, 24 rats underwent occlusion of the left anterior descending coronary artery for 30 min followed by reperfusion. Thirteen rats were rescanned at 24 h post-MI and eleven rats at 2 wk post-MI. Next, rats were euthanized, and histological analysis for MI size was performed. Echocardiographic scans were postprocessed by a layer-specific speckle tracking program to measure the peak circumferential strain (S C peak ) at the endocardium, midlayer, and epicardium as well as total wall thickness S C peak . Linear regression for MI size versus S C peak showed that the slope was steeper for the endocardium compared with the other layers (P Ͻ 0.001), meaning that the endocardium was more sensitive to MI size than the other layers. Moreover, receiver operating characteristics analysis yielded better sensitivity and specificity in the detection of MI using endocardial S C peak instead of total wall thickness S C peak at 24 h post-MI (P Ͻ 0.05) but not 2 wk later. In conclusion, at acute stages of MI, before collagen deposition, scar tissue formation, and remodeling have occurred, damage may be nontransmural, and thus the use of endocardial S C peak is advantageous over total wall thickness S C peak . speckle tracking; transmurality; myocardial viability; left ventricular function THE MYOCARDIAL LAYERS contribute differently to deformation of the left ventricle (LV) at the normal state (4,8,11,23,29), during wall motion abnormalities (1,6,24), and particularly during myocardial infarction (MI) (6). Since nontransmural MI is associated with a high risk for mortality (21), it is essential to identify it at its early stages. The identification of nontransmural MI is challenging, since the myocardial injury is heterogeneous within the myocardial layers (13,15,35), where usually nontransmural MI affects the endocardium first (35).Therefore, the viable layers cause the injured layers to passively contract and move (i.e., tethering). Tethering makes it difficult to identify the MI using the traditional speckle tracking echocardiography (STE) method. The STE method is an angle-independent tool developed for the automatic evaluation of LV regional function (25, 26, 37) by tracking speckle movement in two-dimensional grayscale echocardiographic cine loops (34). The STE is advantageous, among other ...

Following acute myocardial infarction (MI), early and successful reperfusion is the most effective strategy for reducing infarct size and improving the clinical outcome. However, immediate restoration of blood flow to the ischemic zone results in myocardial damage, defined as “reperfusion‐injury”. Whereas we previously reported that TVP1022 (the S‐isomer of rasagiline, FDA‐approved anti‐Parkinson drug) decreased infarct size 24 h post ischemia reperfusion (I/R) in rats, in this study we investigated the chronic cardioprotective efficacy of TVP1022 14 days post‐I/R. To simulate the clinical settings of acute MI followed by reperfusion therapy, we employed a rat model of left anterior descending artery occlusion for 30 min followed by reperfusion and a follow‐up for 14 days. TVP1022 was initially administered postocclusion–prereperfusion, followed by chronic daily administrations. Cardiac performance and remodeling were evaluated using customary and advanced echocardiographic methods, hemodynamic measurements by Millar Mikro‐Tip® catheter, and histopathological techniques. TVP1022 administration markedly decreased the remodeling process as illustrated by attenuation of left ventricular enlargement and cardiac hypertrophy (both at the whole heart and the cellular level). Furthermore, TVP1022 inhibited cardiac fibrosis and reduced ventricular BNP levels. Functionally, TVP1022 treatment preserved cardiac wall motion. Specifically, the echocardiographic and most of the direct hemodynamic measures were pronouncedly improved by TVP1022. Collectively, these findings indicate that TVP1022 provides prominent cardioprotection against I/R injury and post‐MI remodeling in this I/R model.