Dilatometry: a powerful tool for the study of defects in ultrafine-grained metals

Vacancies, dislocations, and interfaces are structural defects that are deliberately introduced into solids during grain refinement processes based on severe plastic deformation (SPD). Specific combinations of these defects determine the improved mechanical properties of the obtained ultrafine-grained materials. High-precision, non-equilibrium dilatometry, i.e., measurement of the irreversible macroscopic length change upon defect annealing, provides a powerful technique for the characterization and the study of the kinetics of these defects. It is applied to determine absolute concentrations of vacancies, to characterize dislocation processes, and to assess grain boundary excess volume in pure, FCC and BCC ultrafine-grained metals processed by SPD.     

Investigation of Optimal Control Problems Governed by a Time-Dependent Kohn-Sham Model

A viable way to develop optimal control strategies for multi-particle quantum systems is to consider the framework of time-dependent density functional theory (TDDFT), where low-dimensional nonlinear Schrödinger models are developed to compute the electronic density of related high-dimensional linear Schrödinger equations. Among these models, the Kohn-Sham TDDFT system allows to accommodate control mechanisms in the same potentials that appear in the original multi-dimensional Schrödinger equations, thus allowing a physical interpretation and a laboratory implementation. The purpose of this paper is the mathematical analysis of optimal control problems governed by the time-dependent Kohn-Sham (TDKS) equations including a control potential that has the purpose to drive the evolution of the electron density to perform given tasks. For the resulting optimal control problems, existence of optimal solutions is proved and their characterization as solutions of TDKS optimality systems is investigated.     

Recrystallization kinetics of ultrafine-grained Ni studied by dilatometry

The release of excess volume upon recrystallization of ultrafine-grained Ni deformed by high-pressure torsion was measured with a high-precision difference-dilatometer employing constant heating rates in the range from 0.3 to 10 K min^?1. The kinetics of the recrystallization process was analyzed according to the Johnson–Mehl–Avrami–Kolmogorov theory adapted to the case of constant heating rates. An effective Avrami exponent of 2 and a value of 1.20 eV for the activation energy of recrystallization was determined. Analysis by the Kissinger method yielded the same result for the activation energy.     

Structure functional expression and spatial distribution of a cloned cDNA encoding a rat 5-HT1D-like receptor

Using polymerase chain reaction (PCR) a complementary DNA (cDNA) encoding a 5-hydroxytryptamine (5-HT) receptor was isolated from rat forebrain. The amplified cDNA specifies an open reading frame of 374 amino acids comprising seven putative transmembrane regions. Expression of the cloned cDNA in human embryonic kidney cells (HEK 293) was used to establish the pharmacological profile of the encoded receptor polypeptide. Membranes containing the cloned receptor showed high affinity binding of [3H]-5-HT. Competition binding experiments with a variety of serotonin receptor ligands displayed a rank order of affinities corresponding to a 5-HT1D subtype: 5-CT > 5-HT = metergoline > CGS 12066 > methysergide > sumatriptan > mianserin = (-)alpha-Me-5-HT = yohimbine > 8-OH-DPAT > or = rauwolscine > spiperone > DOI > propranolol > or = 2-Me-5-HT > or = ICS 205930. Ketanserin and ritanserin displaced [3H]-5-HT-binding in a biphasic manner. In situ hybridization revealed highest expression of the corresponding mRNA in the pyramidal layer of the olfactory tubercle and the nucleus caudatus and accumbens.     

Deletion of glutamate receptor-A (GluR-A) AMPA receptor subunits impairs one-trial spatial memory.

Genetically modified mice lacking the glutamate receptor A (GluR-A) subunit of the AMPA receptor (GluR-A-/- mice) display normal spatial reference memory but impaired spatial working memory (SWM). This study tested whether the SWM impairment in these mice could be explained by a greater sensitivity to within-session proactive interference. The SWM performance of GluR-A-/- and wild-type mice was assessed during nonmatching-to-place testing under conditions in which potential proactive interference from previous trials was reduced or eliminated. SWM was impaired in GluR-A-/- mice, both during testing with pseudotrial-unique arm presentations on the radial maze and when conducting each trial on a different 3-arm maze, each in a novel testing room. Experimentally naive GluR-A-/- mice also exhibited chance performance during a single trial of spontaneous alternation. This 1-trial spatial memory deficit was present irrespective of the delay between the sample information and the response choice (0 or 45 min) and the length of the sample phase (0.5 or 5 min). These results imply that the SWM deficit in GluR-A-/- mice is not due to increased susceptibility to proactive interference. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

A Comparison of GluR-A-Deficient and Wild-Type Mice on a Test Battery Assessing Sensorimotor, Affective, and Cognitive Behaviors.

Previous studies have demonstrated a spatial working memory deficit in glutamate receptor (GluR)-A (GluR1) AMPA receptor subunit knockout mice. The present study evaluated male and female wild-type and GluR-A/ mice on a test battery that assessed sensorimotor, affective, and cognitive behaviors. Results revealed a behavioral phenotype more extensive than previously described. GluR-A/ mice were hyperactive, displayed a subtle lack of motor coordination, and were generally more anxious than wild-type controls. In addition, they showed a deficit in spontaneous alternation, consistent with previous reports of a role for GluR-A-dependent plasticity in hippocampus-dependent, spatial working memory. Although changes in motor coordination or anxiety cannot explain the dissociations already reported within the spatial memory domain, it is clear that they could significantly affect interpretation of results obtained in other kinds of behavioral tasks. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Importance of the intracellular domain of NR2 subunits for NMDA receptor function in vivo

The definitive function of pancreatic polypeptide in mammalian physiology remains unknown. The identification of specific PP target tissues should be helpful to further investigations into the possible regulatory actions of this peptide. An in vivo radioreceptor assay was used in the rat to locate potential binding sites of I(125) bovine PP. In vitro, high concentrations of unlabeled hormone competitively inhibit binding to receptors by low concentrations of labeled hormone. In vivo studies showed that, in the presence of concentrated unlabeled pancreatic polypeptide, labeled PP distributes between the plasma and interstitial fluid. When excess unlabeled PP is replaced with saline in the companion animals, the labeled peptide appears to distribute in a volume that exceeds the combined plasma volume and interstitial fluid volume of the tissue. Using this in vivo receptor assay, the distribution volume that exceeds the anatomic extracellular volume has been identified as the receptor compartment. With this assay we demonstrated in the rat specific and displaceable PP binding to the ductus choledochus, duodenum, ileum, and adrenal gland. The NVV determined in the adrenal gland of experimental animals was 3.9 times greater than that found in the control group. Binding was rapid and was displaced only by excess unlabeled pancreatic polypeptide. Neither excess insulin nor excess neuropeptide Y significantly reduced this binding.     

The AMPA receptor subunit GluR-B in its Q/R site-unedited form is not essential for brain development and function

Calcium permeability of L-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate receptors (AMPARs) in excitatory neurons of the mammalian brain is prevented by coassembly of the GluR-B subunit, which carries an arginine (R) residue at a critical site of the channel pore. The codon for this arginine is created by site-selective adenosine deamination of an exonic glutamine (Q) codon at the pre-mRNA level. Thus, central neurons can potentially control the calcium permeability of AMPARs by the level of GluR-B gene expression as well as by the extent of Q/R-site editing, which in postnatal brain, positions the R codon into >99% of GluR-B mRNA. To study whether the small amount of unedited GluR-B is of functional relevance, we have generated mice carrying GluR-B alleles with an exonic arginine codon. We report that these mutants manifest no obvious deficiencies, indicating that AMPAR-mediated calcium influx into central neurons can be solely regulated by the levels of Q/R site-edited GluR-B relative to other AMPAR subunits. Notably, a targeted GluR-B gene mutant with 30% reduced GluR-B levels had 2-fold higher AMPAR-mediated calcium permeability in hippocampal pyramidal cells with no sign of cytotoxicity. This constitutes proof in vivo that elevated calcium influx through AMPARs need not generate pathophysiological consequences.