What determines the Czech land market prices? Some regional findings

The paper deals with the analysis of market land prices that were collected from land purchased contracts in the Czech Republic. Regression model was used to identify determinants explaining variability of market prices between 2008 and 2009. It was found out that type of plantation, region, type of buyers, plot size, distance to regional city or number of parcels play significant role. These factors explain more than a half of variance in land price. Quality of land that was expressed through administrative price has significant effect on market price. Yet, such effect became less import in regions nearby cities (e.g. Prague and Olomouc), where the market land price is significantly influenced by the distance to the district city. Land reform, however has not been confirmed to stimulate higher prices for sellers. It is reasonable to expect that part of the remaining variation could still be accounted for by non-random variables.Land, market price, administrative price, regression model, region., Land Economics/Use, GA, IN,

The Effects of Tooth Winding Usage

The article deals with tooth windings used forpermanent magnet machinery, their analyses and aftereffectsof their usage. The article discusses basic tooth windingproperties, possibilities of examination of generatedmagnetic field and it studies the impact on the machinecharacteristics. A case study of a designed traction machineequipped with the tooth winding is presented for the purposeof result comparison

Synaptic nanomodules underlie the organization and plasticity of spine synapses.

Experience results in long-lasting changes in dendritic spine size, yet how the molecular architecture of the synapse responds to plasticity remains poorly understood. Here a combined approach of multicolor stimulated emission depletion microscopy (STED) and confocal imaging in rat and mouse demonstrates that structural plasticity is linked to the addition of unitary synaptic nanomodules to spines. Spine synapses in vivo and in vitro contain discrete and aligned subdiffraction modules of pre- and postsynaptic proteins whose number scales linearly with spine size. Live-cell time-lapse super-resolution imaging reveals that NMDA receptor-dependent increases in spine size are accompanied both by enhanced mobility of pre- and postsynaptic modules that remain aligned with each other and by a coordinated increase in the number of nanomodules. These findings suggest a simplified model for experience-dependent structural plasticity relying on an unexpectedly modular nanomolecular architecture of synaptic proteins

Activation of Alpha7 Subunit Containing Nicotinic Acetylcholine Receptors Mediates Cell Death of Neurons in the Avian Ciliary Ganglion

Programmed cell death is a widespread phenomenon in the developing nervous system. During early development, neurons are initially produced in excess and up to 70% of them are eliminated in later stages of development, during a period of synapse formation with their targets. However, the mechanisms that initiate the death of neurons are not clear. In the avian ciliary ganglion, neurons go through the period of target-dependent cell loss between E8 and E14; however, almost all neurons in the ganglion are prevented from dying by the chronic in ovo treatment with α7-nAChRs specific antagonists, α- bungarotoxin or MLA. Since α7-nAChRs are implicated in the cell death of ciliary ganglion neurons, I tested whether the activation of these receptors directly on the ciliary ganglion neurons facilitates cell death by inducing large increases in intracellular Ca2+. I found that the ciliary ganglion neurons are heterogeneous with respect to their surface α7-nAChR density and, as a result, activation of these receptors by nicotine leads to large increases in [Ca2+]i in some neurons but not in others. Furthermore, immature E8 neurons exhibit slower rates of Ca2+ decay after nicotine stimulation than E13 neurons, suggesting that E8 neurons do not clear [Ca2+]i efficiently and could be more susceptible to Ca2+ overload. Expressing the αbtx that is tethered to the cell membrane via the glycosylphosphatidylinositol anchor (GPIαbtx) in the ciliary ganglion neurons inhibits the increases in [Ca2+]i induced by nicotine through α7-nAChRs specifically. This cellautonomous inhibition of α7-nAChRs prevents cell death of ciliary and choroid neurons. For this to happen, GPIαbtx must be expressed in neurons; the expression of this construct in the surrounding non-neural tissue does not prevent neuronal loss in the ciliary ganglion. Later in development, α7-nAChRs are prevented from inducing cell death by the chicken PSCA molecule that is significantly upregulated in the ciliary ganglion between E8 and E15. The chicken PSCA is neuronal specific molecule that belongs to the Ly-6/neurotoxin superfamily that includes αbtx and lynx1 and compared to other tissues, it is highly expressed in the ciliary ganglion. The expression of the PSCA mRNA in tissues correlates with the expression of α7-nAChR mRNA, suggesting that PSCA modulates the signaling via these receptors. In fact, overexpressing the PSCA in the ciliary ganglion neurons prevents nicotine-induced increases in [Ca2+]i through α7- nAChRs. Misexpressing the PSCA in E8 ciliary ganglion prevents choroid but not ciliary neurons from dying. Therefore afferent inputs can induce cell death by activation of α7- nAChRs in the developing ciliary ganglion by increasing the [Ca2+]i over the threshold for cell death. Upregulation of endogenous prototoxins, such as PSCA, opposes the large increases in [Ca2+]i via α7-nAChRs and prevents these channels from facilitating cell death after the final numbers of neurons have been established. These results indicate that the control of cell death is more complex than originally proposed by the neurotrophic hypothesis and present the mechanism by which cell death in the developing ciliary ganglion is regulated, thus, further highlighting the importance of non-traditional roles of α7-nAChRs during the development of the nervous system

Template-based verification of heap-manipulating programs

We propose a shape analysis suitable for analysis engines that perform automatic invariant inference using an SMT solver. The proposed solution includes an abstract template domain that encodes the shape of a program heap based on logical formulae over bit-vectors. It is based on a points-to relation between pointers and symbolic addresses of abstract memory objects. Our abstract heap domain can be combined with value domains in a straight-forward manner, which particularly allows us to reason about shapes and contents of heap structures at the same time. The information obtained from the analysis can be used to prove reachability and memory safety properties of programs manipulating dynamic data structures, mainly linked lists. The solution has been implemented in 2LS and compared against state-of-the-art tools that perform the best in heap-related categories of the well-known Software Verification Competition (SV-COMP). Results show that 2LS outperforms these tools on benchmarks requiring combined reasoning about unbounded data structures and their numerical contents

Potent spinal parenchymal AAV9-mediated gene delivery by subpial injection in adult rats and pigs.

Effective in vivo use of adeno-associated virus (AAV)-based vectors to achieve gene-specific silencing or upregulation in the central nervous system has been limited by the inability to provide more than limited deep parenchymal expression in adult animals using delivery routes with the most clinical relevance (intravenous or intrathecal). Here, we demonstrate that the spinal pia membrane represents the primary barrier limiting effective AAV9 penetration into the spinal parenchyma after intrathecal AAV9 delivery. We develop a novel subpial AAV9 delivery technique and AAV9-dextran formulation. We use these in adult rats and pigs to show (i) potent spinal parenchymal transgene expression in white and gray matter including neurons, glial and endothelial cells after single bolus subpial AAV9 delivery; (ii) delivery to almost all apparent descending motor axons throughout the length of the spinal cord after cervical or thoracic subpial AAV9 injection; (iii) potent retrograde transgene expression in brain motor centers (motor cortex and brain stem); and (iv) the relative safety of this approach by defining normal neurological function for up to 6 months after AAV9 delivery. Thus, subpial delivery of AAV9 enables gene-based therapies with a wide range of potential experimental and clinical utilizations in adult animals and human patients

Ephrin-B3 controls excitatory synapse density through cell-cell competition for EphBs

Cortical networks are characterized by sparse connectivity, with synapses found at only a subset of axo-dendritic contacts. Yet within these networks, neurons can exhibit high connection probabilities, suggesting that cell-intrinsic factors, not proximity, determine connectivity. Here, we identify ephrin-B3 (eB3) as a factor that determines synapse density by mediating a cell-cell competition that requires ephrin-B-EphB signaling. In a microisland culture system designed to isolate cell-cell competition, we find that eB3 determines winning and losing neurons in a contest for synapses. In a Mosaic Analysis with Double Markers (MADM) genetic mouse model system in vivo the relative levels of eB3 control spine density in layer 5 and 6 neurons. MADM cortical neurons in vitro reveal that eB3 controls synapse density independently of action potential-driven activity. Our findings illustrate a new class of competitive mechanism mediated by trans-synaptic organizing proteins which control the number of synapses neurons receive relative to neighboring neurons

Nanoscale rules governing the organization of glutamate receptors in spine synapses are subunit specific

Heterotetrameric glutamate receptors are essential for the development, function, and plasticity of spine synapses but how they are organized to achieve this is not known. Here we show that the nanoscale organization of glutamate receptors containing specific subunits define distinct subsynaptic features. Glutamate receptors containing GluA2 or GluN1 subunits establish nanomodular elements precisely positioned relative to Synaptotagmin-1 positive presynaptic release sites that scale with spine size. Glutamate receptors containing GluA1 or GluN2B specify features that exhibit flexibility: GluA1-subunit containing AMPARs are found in larger spines, while GluN2B-subunit containing NMDARs are enriched in the smallest spines with neither following a strict modular organization. Given that the precise positioning of distinct classes of glutamate receptors is linked to diverse events including cell death and synaptic plasticity, this unexpectedly robust synaptic nanoarchitecture provides a resilient system, where nanopositioned glutamate receptor heterotetramers define specific subsynaptic regions of individual spine synapses