Laboratory study of electromagnetic initiation of slip

Recently Russian seismologists reported the triggering effect of MHD soundings on microseismic activity in the Central Asia test area.The paper focuses on an experimental test of the possibility of triggering the mechanical instability of a system that is close to critical state by a series of electromagnetic pulses.The mechanical system consisted of two pieces of rock;the upper piece can slip on the fixed supporting sample if the latter one is tilted up to the critical angle.In this state,the triggering of mechanical instability by some weak impact such as electrical pulse became more probable.The slope of support in the experiment is an analogue of tectonic stress in natural conditions.The preliminary experiments,carried out in a dry environment,at the humidity of atmosphere 30-50%,show that a strong EM-pulse induces sliding of a sample of rock (granite,basalt,labradorite)placed on the supporting sample which is inclined at the slope close to,but less than,the critical angle with a probability 0.07

NMDA Receptor Phosphorylation at a Site Affected in Schizophrenia Controls Synaptic and Behavioral Plasticity

Phosphorylation of the NR1 subunit of NMDA receptors (NMDARs) at serine (S) 897 is markedly reduced in schizophrenia patients. However, the role of NR1 S897 phosphorylation in normal synaptic function and adaptive behaviors are unknown. To address these questions, we generated mice in which the NR1 S897 is replaced with alanine (A). This knock-in mutation causes severe impairment in NMDAR synaptic incorporation and NMDAR-mediated synaptic transmission. Furthermore, the phosphomutant animals have reduced AMPA receptor (AMPAR)-mediated synaptic transmission, decreased AMPAR GluR1 subunit in the synapse, and impaired long-term potentiation. Finally, the mutant mice exhibit behavioral deficits in social interaction and sensorimotor gating. Our results suggest that an impairment in NR1 phosphorylation leads to glutamatergic hypofunction that can contribute to behavioral deficits associated with psychiatric disorders

Double-Lepton Polarization Asymmetries and Branching Ratio in B \rar K_{0}^{*}(1430) l^+ l^- transition from Universal Extra Dimension Model

We investigate the B \rar K_{0}^{*}(1430) l^+ l^- transition in the Applequist-Cheng-Dobrescu model in the presence of a universal extra dimension. In particular, we calculate double lepton polarization asymmetries and branching ratio related to this channel and compare the obtained results with the predictions of the standard model. Our analysis of the considered observables in terms of radius $R$ of the compactified extra-dimension as the new parameter of the model show a considerable discrepancy between the predictions of two models in low $\frac{1}{R}$ values.Comment: 12 Pages, 15 Figures and 1 Tabl

B to strange tensor meson transition in a model with one universal extra dimension

We analyze the semileptonic $B\to K_2^*(1430)l^+l^-$ transition in universal extra dimension model. In particular, we present the sensitivity of related observables such as branching ratio, polarization distribution and forward-backward asymmetry to the compactification factor (1/R) of extra dimension. The obtained results from extra dimension model show overall a considerable deviation from the standard model predictions for small values of the compactification factor. This can be considered as an indication for existence of extra dimensions.Comment: 10 Pges, 6 Figures and 2 Table

Laboratory study of electromagnetic initiation of slip

Recently Russian seismologists reported the triggering effect of MHD soundings on microseismic activity in the Central Asia test area.The paper focuses on an experimental test of the possibility of triggering the mechanical instability of a system that is close to critical state by a series of electromagnetic pulses.The mechanical system consisted of two pieces of rock;the upper piece can slip on the fixed supporting sample if the latter one is tilted up to the critical angle.In this state,the triggering of mechanical instability by some weak impact such as electrical pulse became more probable.The slope of support in the experiment is an analogue of tectonic stress in natural conditions.The preliminary experiments,carried out in a dry environment,at the humidity of atmosphere 30-50%,show that a strong EM-pulse induces sliding of a sample of rock (granite,basalt,labradorite)placed on the supporting sample which is inclined at the slope close to,but less than,the critical angle with a probability 0.07

Estradiol modulation of phenylephrine-induced excitatory responses in ventromedial hypothalamic neurons of female rats

Estrogens act within the ventromedial nucleus of the hypothalamus (VMN) to facilitate lordosis behavior. Estradiol treatment in vivo induces α1b-adrenoreceptor mRNA and increases the density of α1B-adrenoreceptor binding in the hypothalamus. Activation of hypothalamic α1-adrenoceptors also facilitates estrogen-dependent lordosis. To investigate the cellular mechanisms of adrenergic effects on VMN neurons, whole-cell patch-clamp recordings were carried out on hypothalamic slices from control and estradiol-treated female rats. In control slices, bath application of the α1-agonist phenylephrine (PHE; 10 μM) depolarized 10 of 25 neurons (40%), hyperpolarized three neurons (12%), and had no effect on 12 neurons (48%). The depolarization was associated with decreased membrane conductance, and this current had a reversal potential close to the K+ equilibrium potential. The α1b-receptor antagonist chloroethylclonidine (10 μM) blocked the depolarization produced by PHE in all cells. From estradiol-treated rats, significantly more neurons in slices depolarized (71%) and fewer neurons showed no response (17%) to PHE. PHE-induced depolarizations were significantly attenuated with 4-aminopyridine (5 mM) but unaffected by tetraethylammonium chloride (20 mM) or blockers of Na+ and Ca2+ channels. These data indicate that α1-adrenoceptors depolarize VMN neurons by reducing membrane conductance for K+. Estradiol amplifies α1b-adrenergic signaling by increasing the proportion of VMN neurons that respond to stimulation of α1b-adrenergic receptors, which is expected in turn to promote lordosis. © 2008 by The National Academy of Sciences of the USA

Human P301L-Mutant Tau Expression in Mouse Entorhinal-Hippocampal Network Causes Tau Aggregation and Presynaptic Pathology but No Cognitive Deficits

Accumulation of hyperphosphorylated tau in the entorhinal cortex (EC) is one of the earliest pathological hallmarks in patients with Alzheimer's disease (AD). It can occur before significant Aβ deposition and appears to "spread" into anatomically connecte