We assessed the contribution of well-defined RNA elements in the 3′UTR of DENV-2 to viral translation using a virus-induced reporting gene
system and deoxyribozymes (DRzs) targeting the 3′UTR of the DENV-2 genome. Results show that mRNAs carrying a deletion of repeated conserved sequence (RCS2)-CS2 are translated less efficiently than wild type mRNAs. However, mRNAs with a deletion of CS1-stem loop (SL) are translated more efficiently. Thus, CS1-SL and RCS2-CS2 may have different effects on translational regulation. Additionally, the translation-suppressing effect of CS1-SL or the SL element is further confirmed in DENV-2-infected cells using DRzs. Mutagenesis studies show that, rather than the secondary structure, nucleotides 1.0663-10677 and 10709-10723 are responsible for translational suppression of SL. Overall, our results demonstrate Epigenetic animal study that sequences and elements within the DENV-2 3′UTR regulate viral translation.”
“Acquired epilepsy (AE) is characterized by spontaneous recurrent seizures and long-term changes that occur in surviving neurons following an injury such as status epilepticus (SE). Long-lasting alterations in hippocampal Ca2+ homeostasis have been observed in both in vivo and in Selleck VS-6063 vitro models of AE. One
major regulator of Ca2+ homeostasis is the neuronal calcium binding protein, calbindin-D28k that serves to buffer and transport Ca2+, ions. This study evaluated the expression of hippocampal calbindin levels in the rat pilocarpine model of AE. Calbindin protein expression was reduced over 50% in the hippocampus in epileptic animals. This decrease was observed in the pyramidal layer of CA1, stratum lucidum of CA3, hilus, and stratum granulosum and stratum moleculare of the dentate gyrus when corrected for cell loss. Furthermore, calbindin levels in individual neurons were also significantly reduced. In addition, the expression of calbindin mRNA was decreased in epileptic animals. Time course studies demonstrated that decreased calbindin expression was initially present 1 month following pilocarpine-induced SE and tasted for up to 2 years after the initial episode of SE. The results
indicate that calbindin is essentially HM781-36B Protein Tyrosine Kinase inhibitor permanently decreased in the hippocampus in AE. This decrease in hippocampal calbindin may be a major contributing factor underlying some of the plasticity changes that occur in epileptogenesis and contribute to the alterations in Ca2+ homeostasis associated with AE. (c) 2008 Elsevier B.V. All rights reserved.”
“Bojsen-Moller J, Losnegard T, Kemppainen J, Viljanen T, Kalliokoski KK, Hallen J. Muscle use during double poling evaluated by positron emission tomography. J Appl Physiol 109: 1895-1903, 2010. First published October 14, 2010; doi: 10.1152/japplphysiol.00671.2010.-Due to the complexity of movement in cross-country skiing (XCS), the muscle activation patterns are not well elucidated.