On Free Quotients of Complete Intersection Calabi-Yau Manifolds

In order to find novel examples of non-simply connected Calabi-Yau threefolds, free quotients of complete intersections in products of projective spaces are classified by means of a computer search. More precisely, all automorphisms of the product of projective spaces that descend to a free action on the Calabi-Yau manifold are identified.Comment: 39 pages, 3 tables, LaTe

Involvement of the Metabotropic Glutamate Receptor mGluR5 in NMDA Receptor-Dependent, Learning-Facilitated Long-Term Depression in CA1 Synapses

Learning-facilitated synaptic plasticity describes the ability of hippocampal synapses to respond with persistent synaptic plasticity to the coupling of weak afferent stimulation, which is subthreshold for the induction of plasticity, with a spatial learning experience. The metabotropic glutamate receptor subtype 5 (mGluR5) is critically involved in enabling the persistency of multiple forms of hippocampal synaptic plasticity. We compared the effects of pharmacological allosteric antagonism of mGluR5 in learning-facilitated plasticity with plasticity that had been induced solely by patterned afferent stimulation of the Schaffer collateral pathway to the CA1 stratum radiatum of adult freely behaving rats. Intracerebroventricular injection of the selective mGluR5 antagonist 2-methyl-6-(phenylethynyl)pyridine (MPEP) had no effect on basal synaptic transmission but significantly prevented both long-term depression (LTD) elicited by electrical stimulation and LTD facilitated by novel object-place configuration learning. NMDA receptor antagonism also prevented learning-facilitated LTD. Habituation to the objects was prevented by MPEP application. Whereas reexposure to the object-place configuration (after 7 days) failed to facilitate LTD in control animals, those who had been treated previously with MPEP expressed LTD, suggesting that inhibition of learning contributed to the initial prevention of LTD. These data support a pivotal role for mGluR5 in both hippocampal LTD and the acquisition of object-place configurations

Forest regeneration on European sheep pasture is an economically viable climate change mitigation strategy

Livestock production uses 37% of land globally and is responsible for 15% of anthropogenic greenhouse gas emissions. Yet livestock farmers across Europe receive billions of dollars in annual subsidies to support their livelihoods. This study evaluates whether diverting European subsidies into the restoration of trees on abandoned farmland represents a cost-effective negative-emissions strategy for mitigating climate change. Focusing on sheep farming in the United Kingdom, and on natural regeneration and planted native forests, we show that, without subsidies, sheep farming is not profitable when farmers are paid for their labour. Despite the much lower productivity of upland farms, upland and lowland farms are financially comparable per hectare. Conversion to 'carbon forests' is possible via natural regeneration when close to existing trees, which are seed sources. This strategy is financially viable without subsidies, meeting the net present value of poorly performing sheep farming at a competitive $4/tCO2eq. If tree planting is required to establish forests, then ~$55/tCO2eq is needed to break-even, making it uneconomical under current carbon market prices without financial aid to cover establishment costs. However, this break-even price is lower than the theoretical social value of carbon ($68/tCO2eq), which represents the economic cost of CO2 emissions to society. The viability of land-use conversion without subsidies therefore depends on low farm performance, strong likelihood of natural regeneration, and high carbon-market price, plus overcoming potential trade-offs between the cultural and social values placed on pastoral livestock systems and climate change mitigation. The morality of subsidising farming practices that cause high greenhouse gas emissions in Europe, whilst spending billions annually on protecting forest carbon in less developed nations to slow climate change is questionable

A Mismatch-Based Model for Memory Reconsolidation and Extinction in Attractor Networks

The processes of memory reconsolidation and extinction have received increasing attention in recent experimental research, as their potential clinical applications begin to be uncovered. A number of studies suggest that amnestic drugs injected after reexposure to a learning context can disrupt either of the two processes, depending on the behavioral protocol employed. Hypothesizing that reconsolidation represents updating of a memory trace in the hippocampus, while extinction represents formation of a new trace, we have built a neural network model in which either simple retrieval, reconsolidation or extinction of a stored attractor can occur upon contextual reexposure, depending on the similarity between the representations of the original learning and reexposure sessions. This is achieved by assuming that independent mechanisms mediate Hebbian-like synaptic strengthening and mismatch-driven labilization of synaptic changes, with protein synthesis inhibition preferentially affecting the former. Our framework provides a unified mechanistic explanation for experimental data showing (a) the effect of reexposure duration on the occurrence of reconsolidation or extinction and (b) the requirement of memory updating during reexposure to drive reconsolidation

Campedelli surfaces with fundamental group of order 8

Let S be a Campedelli surface (a minimal surface of general type with p(g) = 0, K-2 = 2), and pi : Y -> S an etale cover of degree 8. We prove that the canonical model (Y) over bar of Y is a complete intersection of four quadrics (Y) over bar = Q(1) boolean AND Q(2) boolean AND Q(3) boolean AND Q(4) subset of P-6. As a consequence, Y is the universal cover of S, the covering group G = Gal(Y/S) is the topological fundamental group pi S-1 and G cannot be the dihedral group D-4 of order 8

Fluoride and Arsenic Exposure Impairs Learning and Memory and Decreases mGluR5 Expression in the Hippocampus and Cortex in Rats

Fluoride and arsenic are two common inorganic contaminants in drinking water that are associated with impairment in child development and retarded intelligence. The present study was conducted to explore the effects on spatial learning, memory, glutamate levels, and group I metabotropic glutamate receptors (mGluRs) expression in the hippocampus and cortex after subchronic exposure to fluoride, arsenic, and a fluoride and arsenic combination in rats. Weaned male Sprague-Dawley rats were assigned to four groups. The control rats drank tap water. Rats in the three exposure groups drank water with sodium fluoride (120 mg/L), sodium arsenite (70 mg/L), and a sodium fluoride (120 mg/L) and sodium arsenite (70 mg/L) combination for 3 months. Spatial learning and memory was measured in Morris water maze. mGluR1 and mGluR5 mRNA and protein expression in the hippocampus and cortex was detected using RT-PCR and Western blot, respectively. Compared with controls, learning and memory ability declined in rats that were exposed to fluoride and arsenic both alone and combined. Combined fluoride and arsenic exposure did not have a more pronounced effect on spatial learning and memory compared with arsenic and fluoride exposure alone. Compared with controls, glutamate levels decreased in the hippocampus and cortex of rats exposed to fluoride and combined fluoride and arsenic, and in cortex of arsenic-exposed rats. mGluR5 mRNA and protein expressions in the hippocampus and mGluR5 protein expression in the cortex decreased in rats exposed to arsenic alone. Interestingly, compared with fluoride and arsenic exposure alone, fluoride and arsenic combination decreased mGluR5 mRNA expression in the cortex and protein expression in the hippocampus, suggesting a synergistic effect of fluoride and arsenic. These data indicate that fluoride and arsenic, either alone or combined, can decrease learning and memory ability in rats. The mechanism may be associated with changes of glutamate level and mGluR5 expression in cortex and hippocampus