Background and Purpose-Ischemic injury can induce neurogenesis in the striatum. Those newborn neurons can express glutamic acid decarboxylase and choline acetyltransferase, markers of GABAergic and cholinergic neurons, respectively. The present study investigated whether these GABAergic and cholinergic new neurons could differentiate into functional cells. Methods-Retrovirus containing the EGFP gene was used to label dividing cells in striatal slices prepared from adult rat brains after middle cerebral artery occlusion. EGFP-targeted immunostaining and immunoelectron microscopy were performed to detect whether newborn neurons could anatomically form neuronal polarity and synapses with pre-existent neurons. Patch clamp recording on acute striatal slices of brains at 6 to 8 weeks after middle cerebral artery occlusion was used to determine whether the newborn neurons could display functional electrophysiological properties. Results-EGFP-expressing (EGFPϩ ) signals could be detected mainly in the cell body in the first 2 weeks. From the fourth to thirteenth weeks after their birth, EGFP ϩ neurons gradually formed neuronal polarity and showed a time-dependent increase in dendrite length and branch formation. EGFP ϩ cells were copositive for NeuN and glutamic acid decarboxylase (EGFP ϩ -NeuN ϩ -GAD 67 ϩ ), MAP-2, and choline acetyltransferase (EGFP ϩ -MAP-2 ϩ -ChAT ϩ ). They also expressed phosphorylated synapsin I (EGFP ϩ -p-SYN ϩ ) and showed typical synaptic structures comprising dendrites and spines. Both GABAergic and cholinergic newborn neurons could fire action potentials and received excitatory and inhibitory synaptic inputs because they displayed spontaneous postsynaptic currents in picrotoxin-and CNQX-inhibited manners. Conclusion-Ischemia-induced newly formed striatal GABAergic and cholinergic neurons could become functionally integrated into neural networks in the brain of adult rats after stroke.
A dielectric elastomer is capable of giant electromechanical actuation but fails at breakdown due to instability under certain conditions with a small deformation. By applying a mechanical pre-stretch, one obtains a stabilized large actuation. In this paper, we measured the dielectric constant and critical voltage of a polyacrylic dielectric elastomer subjected to both equal and unequal biaxial stretch, and modelled its actuation by employing the Gent strain energy function with a microscopic view to characterize the nonlinear stiffening behaviour and the electrostrictive effect in the deformation. The mechanical pre-stretch contributes in several ways to the stabilization of dielectric elastomer, by eliminating the pull-in instability, by generating electrostriction, by improving the breakdown strength, as well as by reducing the membrane thickness which consequently lowers the voltages required for activation.
This paper proposes a free energy model to study the dynamic characteristics of a dielectric elastomer membrane undergoing in-plane deformation, subject to the combined loads of a mechanical press and an electric field. The natural frequency of the small-amplitude perturbation around the state of equilibrium is calculated with focus on the damping effects and the resonance phenomenon. The numerical results, such as the oscillation, phase diagrams and Poincaré maps, are presented to show the influence of the damping on the nonlinear dynamic characteristics of the dielectric elastomer. The numerical results indicate that pre-stresses, damping effects and applied voltages could tune the natural frequency and modify the dynamic behavior of the dielectric elastomer. There is a stability transition when taking the damping effect into account. The damping effect could cause the dynamic responses to constant vibration and decrease the amplitude. These conclusions may guide the exploration of high-performance dielectric elastomers under dynamic mechanical and electrical loads.
Incidence and mortality rates for prostate cancer (PCa) are higher in African-American (AA) men than European American (EA) men, but the biological basis for this disparity is unclear. We carried out a detailed analysis of gene expression changes in PCa compared to their matched benign tissues in a cohort of AA men and compared them to existing data from EA men. In this manner, we identified MNX1 as a novel oncogene upregulated to a relatively greater degree in PCa from AA men. Androgen and AKT signaling play a central role in the pathogenesis of PCa and we found that both of these signaling pathways increased MNX1 expression. MNX1 in turn upregulated lipid synthesis by stimulating expression of SREBP1 and fatty acid synthetase. Our results define MNX1 as a novel targetable oncogene increased in AA PCa that is associated with aggressive disease.
To elucidate whether vascular endothelial growth factor (VEGF) improves stroke-induced striatal neurogenesis, we intraventricularly injected human VEGF(165)-expressive plasmid (phVEGF) mixed with liposome into adult rats after a transient middle cerebral artery occlusion (MCAO). The results showed that EGFP, a reporter protein, positive cells appeared at 2 hr, further enhanced at 4 hr, reached the maximum at 3 days and still remained at 14 days after a single injection. Treatment with phVEGF increased angiogenesis, as indicated by double staining of vWF, a marker of endothelial cells, and 5'-bromodeoxyuridine (BrdU), a marker of cell proliferation. The phVEGF treatment dose-dependently reduced infarct volume of brain at 2 weeks after MCAO. The neuroprotection by VEGF could be obtained when the plasmid was injected within 2 hr after stroke. Moreover, VEGF overexpression significantly increased cell proliferation in the ipsilateral SVZ and the numbers of BrdU(+)-CRMP-4(+) and BrdU(+)-Tuj1(+), two markers of immature newborn neurons, and BrdU(+)-MAP-2(+), a marker of mature newborn neurons, cells in the ipsilateral striatum to MCAO. Present results show that VEGF plasmid treatment after stroke can significantly reduce infarct volume and enhance striatal neurogenesis in adult rat brain. This suggests that VEGF overexpression acquires significant functions of neuronal protection and repair in the injured brain, which provides a possibility to develop a novel therapeutic strategy for the patients with stroke.
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