1,710 research outputs found
Characterization of the yeast flora on the surface of grape berries in Israel
Yeast populations were collected from the surface of berries of three grape cultivars during three seasons, from fruit set to maturity. They were studied by RAPD and ap-PCR, each with two primer pairs. In the population, identical isolates were found only rarely on 13 % of the bunches in 1997 and on 58 % of the berries in 1999. From RAPD and ap-PCR, a dendrogram with clusters of similarity was established. Eleven representatives from clusters of the white yeast dendrogram were identified by traditional methods as 10 different yeast species, one of which has not been isolated from grape berry surfaces before. The population size was smaller for Colombard than for Cabernet Sauvignon and Muscat of Alexandria berries.
Temporal coding at the immature depolarizing gabaergic synapse
In the developing hippocampus, GABA exerts depolarizing and excitatory actions and contributes to the generation of neuronal network driven giant depolarizing potentials (GDPs). Here, we studied spike time coding at immature GABAergic synapses and its impact on synchronization of the neuronal network during GDPs in the neonatal (postnatal days P2-6) rat hippocampal slices. Using extracellular recordings, we found that the delays of action potentials (APs) evoked by synaptic activation of GABA(A) receptors are long (mean, 65 ms) and variable (within a time window of 10-200 ms). During patch-clamp recordings, depolarizing GABAergic responses were mainly subthreshold and their amplification by persistent sodium conductance was required to trigger APs. AP delays at GABAergic synapses shortened and their variability reduced with an increase in intracellular chloride concentration during whole-cell recordings. Negative shift of the GABA reversal potential (EGABA) with low concentrations of bumetanide, or potentiation of GABA(A) receptors with diazepam reduced GDPs amplitude, desynchronized neuronal firing during GDPs and slowed down GDPs propagation. Partial blockade of GABA(A) receptors with bicuculline increased neuronal synchronization and accelerated GDPs propagation. We propose that spike timing at depolarizing GABA synapses is determined by intracellular chloride concentration. At physiological levels of intracellular chloride GABAergic depolarization does not reach the action potential threshold and amplification of GABAergic responses by non-inactivating sodium conductance is required for postsynaptic AP initiation. Slow and variable excitation at GABAergic synapse determines the level of neuronal synchrony and the rate of GDPs propagation in the developing hippocampus. © 2010 Valeeva, Abdullin, Tyzio, Skorinkin, Nikolski, Ben-Ari and Khazipov
Improving BDD Based Symbolic Model Checking with Isomorphism Exploiting Transition Relations
Symbolic model checking by using BDDs has greatly improved the applicability
of model checking. Nevertheless, BDD based symbolic model checking can still be
very memory and time consuming. One main reason is the complex transition
relation of systems. Sometimes, it is even not possible to generate the
transition relation, due to its exhaustive memory requirements. To diminish
this problem, the use of partitioned transition relations has been proposed.
However, there are still systems which can not be verified at all. Furthermore,
if the granularity of the partitions is too fine, the time required for
verification may increase. In this paper we target the symbolic verification of
asynchronous concurrent systems. For such systems we present an approach which
uses similarities in the transition relation to get further memory reductions
and runtime improvements. By applying our approach, even the verification of
systems with an previously intractable transition relation becomes feasible.Comment: In Proceedings GandALF 2011, arXiv:1106.081
Efficient Symmetry Reduction and the Use of State Symmetries for Symbolic Model Checking
One technique to reduce the state-space explosion problem in temporal logic
model checking is symmetry reduction. The combination of symmetry reduction and
symbolic model checking by using BDDs suffered a long time from the
prohibitively large BDD for the orbit relation. Dynamic symmetry reduction
calculates representatives of equivalence classes of states dynamically and
thus avoids the construction of the orbit relation. In this paper, we present a
new efficient model checking algorithm based on dynamic symmetry reduction. Our
experiments show that the algorithm is very fast and allows the verification of
larger systems. We additionally implemented the use of state symmetries for
symbolic symmetry reduction. To our knowledge we are the first who investigated
state symmetries in combination with BDD based symbolic model checking
Galanin Receptor 1 Deletion Exacerbates Hippocampal Neuronal Loss after Systemic Kainate Administration in Mice
Galanin is a neuropeptide with a wide distribution in the central and peripheral nervous systems and whose physiological effects are mediated through three G protein-coupled receptor subtypes, GalR1, GalR2, and GalR3. Several lines of evidence indicate that galanin, as well as activation of the GalR1 receptor, is a potent and effective modulator of neuronal excitability in the hippocampus.In order to test more formally the potential influence of GalR1 on seizure-induced excitotoxic cell death, we conducted functional complementation tests in which transgenic mice that exhibit decreased expression of the GalR1 candidate mRNA underwent kainate-induced status epilepticus to determine if the quantitative trait of susceptibility to seizure-induced cell death is determined by the activity of GalR1. In the present study, we report that reduction of GalR1 mRNA via null mutation or injection of the GalR1 antagonist, galantide, prior to kainate-induced status epilepticus induces hippocampal damage in a mouse strain known to be highly resistant to kainate-induced neuronal injury. Wild-type and GalR1 knockout mice were subjected to systemic kainate administration. Seven days later, Nissl and NeuN immune- staining demonstrated that hippocampal cell death was significantly increased in GalR1 knockout strains and in animals injected with the GalR1 antagonist. Compared to GalR1-expressing mice, GalR1-deficient mice had significantly larger hippocampal lesions after status epilepticus.Our results suggest that a reduction of GalR1 expression in the C57BL/6J mouse strain renders them susceptible to excitotoxic injury following systemic kainate administration. From these results, GalR1 protein emerges as a new molecular target that may have a potential therapeutic value in modulating seizure-induced cell death
NKCC1 downregulation induces hyperpolarizing shift of GABA responsiveness at near term fetal stages in rat cultured dorsal root ganglion neurons
γ-Aminobutyric Acid (GABA) Is an Autocrine Excitatory Transmitter in Human Pancreatic β-Cells
OBJECTIVE: Paracrine signaling via gamma-aminobutyric acid (GABA) and GABA(A) receptors (GABA(A)Rs) has been documented in rodent islets. Here we have studied the importance of GABAergic signaling in human pancreatic islets. RESEARCH DESIGN AND METHODS: Expression of GABA(A)Rs in islet cells was investigated by quantitative PCR, immunohistochemistry, and patch-clamp experiments. Hormone release was measured from intact islets. GABA release was monitored by whole-cell patch-clamp measurements after adenoviral expression of alpha(1)beta(1) GABA(A)R subunits. The subcellular localization of GABA was explored by electron microscopy. The effects of GABA on electrical activity were determined by perforated patch whole-cell recordings. RESULTS: PCR analysis detected relatively high levels of the mRNAs encoding GABA(A)R alpha(2), beta(3,) gamma(2), and pi subunits in human islets. Patch-clamp experiments revealed expression of GABA(A)R Cl(-) channels in 52% of beta-cells (current density 9 pA/pF), 91% of delta-cells (current density 148 pA/pF), and 6% of alpha-cells (current density 2 pA/pF). Expression of GABA(A)R subunits in islet cells was confirmed by immunohistochemistry. beta-Cells secreted GABA both by glucose-dependent exocytosis of insulin-containing granules and by a glucose-independent mechanism. The GABA(A)R antagonist SR95531 inhibited insulin secretion elicited by 6 mmol/l glucose. Application of GABA depolarized beta-cells and stimulated action potential firing in beta-cells exposed to glucose. CONCLUSIONS: Signaling via GABA and GABA(A)R constitutes an autocrine positive feedback loop in human beta-cells. The presence of GABA(A)R in non-beta-cells suggests that GABA may also be involved in the regulation of somatostatin and glucagon secretion
Multifield Dynamics in Higgs-otic Inflation
In Higgs-otic inflation a complex neutral scalar combination of the and
MSSM Higgs fields plays the role of inflaton in a chaotic fashion. The
potential is protected from large trans-Planckian corrections at large inflaton
if the system is embedded in string theory so that the Higgs fields parametrize
a D-brane position. The inflaton potential is then given by a DBI+CS D-brane
action yielding an approximate linear behaviour at large field. The inflaton
scalar potential is a 2-field model with specific non-canonical kinetic terms.
Previous computations of the cosmological parameters (i.e. scalar and tensor
perturbations) did not take into account the full 2-field character of the
model, ignoring in particular the presence of isocurvature perturbations and
their coupling to the adiabatic modes. It is well known that for generic
2-field potentials such effects may significantly alter the observational
signatures of a given model. We perform a full analysis of adiabatic and
isocurvature perturbations in the Higgs-otic 2-field model. We show that the
predictivity of the model is increased compared to the adiabatic approximation.
Isocurvature perturbations moderately feed back into adiabatic fluctuations.
However, the isocurvature component is exponentially damped by the end of
inflation. The tensor to scalar ratio varies in a region ,
consistent with combined Planck/BICEP results.Comment: 35 pages, 11 figure
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