Afferent activity from multifidus
and longissimus muscle spindles was recorded in the L-6 dorsal root in 30 anesthetized cats. To alter movement history, a feedback-controlled motor attached to the L-6 spinous process held (conditioned for 4 s) the L-6 vertebra at an intermediate position or at positions that either lengthened find more or shortened the muscles. With the vertebra returned to the intermediate position, resting spindle discharge was measured over the next 0.5 s (static test) and then during a dynamic test consisting of ramp vertebral movement at four velocities (0.2, 0.5, 1.0, 2.0 mm/s). Spindle activity during the tests was measured relative to hold-intermediate. For both tests, hold-long decreased and hold-short increased muscle spindle responsiveness. For the static test
position responsiveness was not different among the velocity protocols for either hold-long or hold-short (P = 0.42 and 0.24, respectively). During the dynamic test, hold-long conditioning significantly decreased [F-(3,F-119) = 7.99, P < 0.001] spindle responsiveness to increasing velocity. Mean velocity sensitivity was 4.44, 3.39, and 1.41 (impulses/s)/(mm/s) for the hold-short, hold-intermediate, and hold-long protocols, respectively. The nearly 2.5-fold decrease in velocity sensitivity following hold-long was significantly less than that for either hold-intermediate (P = 0.005) or hold-short conditioning (P < 0.001). Hold-short
conditioning had little effect on velocity responses during the dynamic test [F-(3,F-119) = 0.23, P = 0.87]. In conclusion, only movement histories that GSI-IX supplier stretch but not shorten muscle spindles alter their velocity sensitivity. In the low back, forward flexion and lateral bending postures would likely be the most provocative.”
“Purpose: Atypical teratoid/rhabdoid tumors (AT/RT) are highly aggressive pediatric malignancies characterized by biallelic inactivation of the SMARCB1 tumor suppressor gene. We searched for novel genomic aberrations by investigating the copy number and expression alterations of let-7a3/let-76 microRNA (miRNA) and correlated these with expression of high-mobility group AT-hook 2 (HMGA2) oncoprotein, a target of let-7 miRNA family, in 18 AT/RT samples to elucidate potential roles Selleck Ro 61-8048 of HMGA2 in the pathogenesis of AT/RT.\n\nExperimental Design: Genomic aberrations, let-7a3/let-7b miRNA and HMGA2 expression in AT/RT tissues were identified using quantitative PCR, reverse transcription PCR (RT-PCR), and immunohistochemistry. The impact of let-76 iniRNA on HMGA2 expression and the malignant potential of human rhabdoid tumor cell G401 (SMARCB1(-/-)) were investigated by antisense inhibition and ectopic overexpression studies.\n\nResults: The copy number of let-7a3/let-76 miRNA was substantially decreased in 4 of 11 AT/RT samples.