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More than one million copies of short interspersed elements (SINEs), a class of retrotransposons, are present in the mammalian genomes, particularly within gene-rich genomic regions. Evidence has accumulated that ancient SINE sequences have acquired new binding sites for transcription factors (TFs) through multiple mutations following retrotransposition, and as a result have rewired the host regulatory network during the course of evolution. However, it remains unclear whether currently active SINEs contribute to the expansion of TF binding sites. To study the mobility, expression, and function of SINE copies, we first identified about 2,000 insertional polymorphisms of SINE B1 and B2 families within Mus musculus. Using a novel RNA sequencing method designated as melRNA-seq, we detected the expression of SINEs in male germ cells at both the subfamily and genomic copy levels: the vast majority of B1 RNAs originated from evolutionarily young subfamilies, whereas B2 RNAs originated from both young and old subfamilies. DNA methylation and chromatin immunoprecipitation-sequencing (ChIP-seq) analyses in liver revealed that polymorphic B2 insertions served as a boundary element inhibiting the expansion of DNA hypomethylated and histone hyperacetylated regions, and decreased the expression of neighboring genes. Moreover, genomic B2 copies were enriched at the boundary of various histone modifications, and CTCF, a well-known chromatin boundary protein, bound to > 100 polymorphic and >10,000 non-polymorphic B2 insertions. These results suggest that the currently active B2 copies are mobile boundary elements that can modulate chromatin modifications and gene expression, and are likely involved in epigenomic and phenotypic diversification of the mouse species.

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Purpose: To investigate the sequential changes in heart rate (HR), autonomic nervous activity presented by the spectral analysis of heart rate variability (HRV), hemodynamics and metabolism during massive hemorrhage and progressive hemorrhagic shock in dogs.Methods: Twelve dogs were subjected to acute massive hemorrhage until mean arterial pressure (MAP) reached 50 mmHg. Then bleeding was stopped and they were allowed to reach a plateau phase. They were divided, post hoc, into bradycardic or tachycardic groups according to their HR response to the acute massive hemorrhage. After reaching a plateau phase, the dogs were further bled to keep their MAP around 50 mmHg (progressive hemorrhagic shock). Their heart rate power spectra were quantified into low-frequency (LF) (0.04-0.15 Hz) and high-frequency (HF) (0.15-0.4 Hz) components.Results: In the bradycardic group, both LF and HF increased after massive hemorrhage, but during progressive hemorrhagic shock these components decreased while HR increased. In the tachycardic group, LF increased after massive hemorrhage, but during progressive hemorrhagic shock LF decreased with continuous suppression of HF. Conclusion:Massive hemorrhage caused two types of HR response: bradycardia and tachycardia. The HRV profile showed differential autonomic characteristics, and could be a valuable tool in assessing various degrees of hemorrhagic shock.Objectif : Examiner les changements de fréquence cardiaque (FC), l'activité nerveuse autonome selon l'analyse spectrale de la variabilité de la fréquence cardiaque (VFC), l'hémodynamie et le métabolisme pendant une hémor-ragie massive et un choc hémorragique progressif, chez des chiens.Méthode : Douze chiens ont été soumis à une hémorragie aiguë massive jusqu'à ce que la tension artérielle moyenne (TAM) atteigne 50 mmHg. Puis, on a arrêté le saignement et laissé la pression parvenir à un plateau. On a, en conséquence, réparti les animaux en groupe bradycardie ou tachycardie selon le comportement de la FC pendant l'hémorragie aiguë massive. Un plateau une fois atteint, les chiens ont subi une autre hémorragie pour amener leur TAM autour de 50 mmHg (choc hémorragique progressif). Le spectre de la puissance de la fréquence cardiaque a été quantifié en composantes de basses fréquences (BF) (0,04-0,15 Hz) et de hautes fréquences (HF) (0,15-0,4 Hz).Résultats : Dans le groupe bradycardie, les BF et HF ont augmenté après l'hémorragie massive, mais lors du choc hémorragique progressif, ces composantes ont diminué pendant que la FC augmentait. Dans le groupe tachycardie, les BF ont augmenté après l'hémorragie massive, mais lors du choc, elles ont baissé en même temps que survenait la suppression continue des HF.Conclusion : L'hémorragie massive a causé deux types de réaction de la FC : la bradycardie et la tachycardie. Le profil de VFC a affiché des caractéristiques autonomes différentielles, ce qui en fait un outil valable pour éva-luer différents degrés de choc hémorragique.

Power spectra of heart rate variability (HRV) and blood pressure variability (BPV) were computed using the fast Fourier transformation. The HRV and BPV showed their differential characteristics during hemorrhage, isoflurane anesthesia, and retransfusion, and would help to assess changes in autonomic nervous system and preload under mechanical ventilation.

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