59 research outputs found

    Game saturation of intersecting families

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    We consider the following combinatorial game: two players, Fast and Slow, claim kk-element subsets of [n]={1,2,...,n}[n]=\{1,2,...,n\} alternately, one at each turn, such that both players are allowed to pick sets that intersect all previously claimed subsets. The game ends when there does not exist any unclaimed kk-subset that meets all already claimed sets. The score of the game is the number of sets claimed by the two players, the aim of Fast is to keep the score as low as possible, while the aim of Slow is to postpone the game's end as long as possible. The game saturation number is the score of the game when both players play according to an optimal strategy. To be precise we have to distinguish two cases depending on which player takes the first move. Let gsatF(In,k)gsat_F(\mathbb{I}_{n,k}) and gsatS(In,k)gsat_S(\mathbb{I}_{n,k}) denote the score of the saturation game when both players play according to an optimal strategy and the game starts with Fast's or Slow's move, respectively. We prove that Ωk(nk/35)gsatF(In,k),gsatS(In,k)Ok(nkk/2)\Omega_k(n^{k/3-5}) \le gsat_F(\mathbb{I}_{n,k}),gsat_S(\mathbb{I}_{n,k}) \le O_k(n^{k-\sqrt{k}/2}) holds

    Febrile seizures and mechanisms of epileptogenesis: insights from an animal model.

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    Temporal lobe epilepsy (TLE) is the most prevalent type of human epilepsy, yet the causes for its development, and the processes involved, are not known. Most individuals with TLE do not have a family history, suggesting that this limbic epilepsy is a consequence of acquired rather than genetic causes. Among suspected etiologies, febrile seizures have frequently been cited. This is due to the fact that retrospective analyses of adults with TLE have demonstrated a high prevalence (20-->60%) of a history of prolonged febrile seizures during early childhood, suggesting an etiological role for these seizures in the development of TLE. Specifically, neuronal damage induced by febrile seizures has been suggested as a mechanism for the development of mesial temporal sclerosis, the pathological hallmark of TLE. However, the statistical correlation between febrile seizures and TLE does not necessarily indicate a causal relationship. For example, preexisting (genetic or acquired) 'causes' that result independently in febrile seizures and in TLE would also result in tight statistical correlation. For obvious reasons, complex febrile seizures cannot be induced in the human, and studies of their mechanisms and of their consequences on brain molecules and circuits are severely limited. Therefore, an animal model was designed to study these seizures. The model reproduces the fundamental key elements of the human condition: the age specificity, the physiological temperatures seen in fevers of children, the length of the seizures and their lack of immediate morbidity. Neuroanatomical, molecular and functional methods have been used in this model to determine the consequences of prolonged febrile seizures on the survival and integrity of neurons, and on hyperexcitability in the hippocampal-limbic network. Experimental prolonged febrile seizures did not lead to death of any of the seizure-vulnerable populations in hippocampus, and the rate of neurogenesis was also unchanged. Neuronal function was altered sufficiently to promote synaptic reorganization of granule cells, and transient and long-term alterations in the expression of specific genes were observed. The contribution of these consequences of febrile seizures to the epileptogenic process is discussed

    Hippocampal pyramidal cells: the reemergence of cortical lamination

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    The increasing resolution of tract-tracing studies has led to the definition of segments along the transverse axis of the hippocampal pyramidal cell layer, which may represent functionally defined elements. This review will summarize evidence for a morphological and functional differentiation of pyramidal cells along the radial (deep to superficial) axis of the cell layer. In many species, deep and superficial sublayers can be identified histologically throughout large parts of the septotemporal extent of the hippocampus. Neurons in these sublayers are generated during different periods of development. During development, deep and superficial cells express genes (Sox5, SatB2) that also specify the phenotypes of superficial and deep cells in the neocortex. Deep and superficial cells differ neurochemically (e.g. calbindin and zinc) and in their adult gene expression patterns. These markers also distinguish sublayers in the septal hippocampus, where they are not readily apparent histologically in rat or mouse. Deep and superficial pyramidal cells differ in septal, striatal, and neocortical efferent connections. Distributions of deep and superficial pyramidal cell dendrites and studies in reeler or sparsely GFP-expressing mice indicate that this also applies to afferent pathways. Histological, neurochemical, and connective differences between deep and superficial neurons may correlate with (patho-) physiological phenomena specific to pyramidal cells at different radial locations. We feel that an appreciation of radial subdivisions in the pyramidal cell layer reminiscent of lamination in other cortical areas may be critical in the interpretation of studies of hippocampal anatomy and function

    Circuit-based interrogation of sleep control.

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    Sleep is a fundamental biological process observed widely in the animal kingdom, but the neural circuits generating sleep remain poorly understood. Understanding the brain mechanisms controlling sleep requires the identification of key neurons in the control circuits and mapping of their synaptic connections. Technical innovations over the past decade have greatly facilitated dissection of the sleep circuits. This has set the stage for understanding how a variety of environmental and physiological factors influence sleep. The ability to initiate and terminate sleep on command will also help us to elucidate its functions within and beyond the brain

    Connecting the data landscape of long-term ecological studies: The SPI-Birds data hub

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    The integration and synthesis of the data in different areas of science is drastically slowed and hindered by a lack of standards and networking programmes. Long-term studies of individually marked animals are not an exception. These studies are especially important as instrumental for understanding evolutionary and ecological processes in the wild. Furthermore, their number and global distribution provides a unique opportunity to assess the generality of patterns and to address broad-scale global issues (e.g. climate change). To solve data integration issues and enable a new scale of ecological and evolutionary research based on long-term studies of birds, we have created the SPI-Birds Network and Database (www.spibirds.org)\u2014a large-scale initiative that connects data from, and researchers working on, studies of wild populations of individually recognizable (usually ringed) birds. Within year and a half since the establishment, SPI-Birds has recruited over 120 members, and currently hosts data on almost 1.5 million individual birds collected in 80 populations over 2,000 cumulative years, and counting. SPI-Birds acts as a data hub and a catalogue of studied populations. It prevents data loss, secures easy data finding, use and integration and thus facilitates collaboration and synthesis. We provide community-derived data and meta-data standards and improve data integrity guided by the principles of Findable, Accessible, Interoperable and Reusable (FAIR), and aligned with the existing metadata languages (e.g. ecological meta-data language). The encouraging community involvement stems from SPI-Bird's decentralized approach: research groups retain full control over data use and their way of data management, while SPI-Birds creates tailored pipelines to convert each unique data format into a standard format. We outline the lessons learned, so that other communities (e.g. those working on other taxa) can adapt our successful model. Creating community-specific hubs (such as ours, COMADRE for animal demography, etc.) will aid much-needed large-scale ecological data integration

    Fungi Parasitizing Powdery Mildew Fungi: Ampelomyces Strains as Biocontrol Agents Against Powdery Mildews

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    Among the mycoparasites, Ampelomyces strains are studied in detail, particularly regarding their use as biocontrol agents (BCAs) of powdery mildew (PM) fungi, including their potential to replace conventional agrochemicals. Ampelomyces strains are characterized morphologically; their ribosomal DNA internal transcribed spacer (rDNA-ITS) regions and actin gene (ACT) fragments were sequenced and their mycoparasitic activity was analyzed. In the interaction between Ampelomyces strains and PM fungi, the spores of the mycoparasites germinate on plant leaves, and their hyphae then penetrate the hyphae of PM fungi. Ampelomyces hyphae continue their growth internally, initiating the atrophy of PM conidiophores and eventually their complete collapse. Following the successful destruction of PM hyphae by Ampelomyces, the mycoparasite produces new intracellular pycnidia in PM conidiophores. The progeny spores released by mature pycnidia become the sources of subsequent infections of intact PM hyphae. As a result, the number of Ampelomyces-inoculated PM colonies gradually declines, and the conidial release of PM colonies is inhibited after the first treatment. Almost all conidiophores of 5- and 10-day-old Ampelomyces-inoculated PM colonies undergo complete atrophy or collapse. Methodological advances and in-depth analyses of the Ampelomyces–PM interaction were recently published. In this review, we summarize the genetic and phylogenetic diversity, the timing of mycoparasitism and pycnidiogenesis, the results of quantitative and visual analyses using electrostatic and digital microscopy technologies, the PM biocontrol potential of Ampelomyces, and the potential commercialization of the mycoparasites. The information provided herein can support further biocontrol and ecological studies of Ampelomyces mycoparasites

    What mechanisms are involved in cabbage-clover intercropping and a further proof of the 'host plant quality' hypothesis

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    Over 10 years of field trials show reductions of most of the pests in Brassicas undersown by clover. The pest-reducing effects are due to the 'appropriate / inappropriate landings' hypothesis (Finch, 1996), and the 'host plant quality' hypothesis (Theunissen, 1994). To find out the mechanisms within the 'host plant quality' hypothesis in the most promising intercropping (collards undersown by clover) glasshouse experiments were conducted to see whether intercropping influences the mean relative growth rate, fecundity and time of maturity of Myzus persicae (Sulzer) (Homoptera: Aphididae) a common pest of Brassicas. The treatment modelling intercropping showed the smallest mean relative growth rate, delayed the maturity and slowed down the growth of cabbages. The treatment modelling monocropping showed the highest mean relative growth rate and the maturity was reached earlier. These results may indicate that intercropping delays the growth of settled aphid populations, giving another proof that in the case of clover undersown cabbages the 'host plant quality' hypothesis is likely to be acting. The differences between treatments where the roots of clover and cabbages were separated and allowed to grow together suggest that the effect is via the roots by competition. &nbsp

    Novel calretinin and reelin expressing neuronal population includes Cajal-Retzius-type cells in the neocortex of adult pigs

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    Cajal-Retzius cells and their secreted product reelin are essential for the lamination of the cerebral cortex. In all species studied to date Cajal-Retzius cells form a transient neuronal population that almost completely disappears from the neocortex postnatally. Recently, in the hippocampal for- mation of adult domestic pig, we have found a large calreti- nin- and reelin-immunoreactive cell population that morpho- logically corresponded to Cajal-Retzius cells. In the present study, we examined calretinin- and reelin- immunoreactive neurons in layer I of the prefrontal, temporal, parietal and occipital neocortical areas of newborn, young adult and adult domestic pigs. Large numbers of bipolar or fusiform calretinin-positive cells were found in the upper half of layer I in all examined age groups. The morphology of these neurons resembled that of the Cajal-Retzius cells. Layer I was occupied by a dense calretinin-positive axonal plexus that was similar to the previously described axons of Cajal-Retzius cells in other species. In a similar location, where calretinin-positive cells occurred in layer I, large numbers of reelin-immunoreactive cells were found in all examined age groups. In addition, reelin colocalized with calretinin in layer I neurons. The number of calretinin and reelin-positive neurons decreased from 1 day to one year, but calretinin-positive Cajal-Retzius-type cells still comprised a remarkable large population in 12-month-old animals. Correlated light and electron microscopic examination of calretinin-labeled Cajal-Retzius-type cells indicated that these cells are integrated in the synaptic circuitry of the neocortex. Our results suggest that Cajal-Retzius cells do not disap- pear inevitably from the mature neocortex in all mammalian species. The function of this cell type is not known, but late persisting Cajal-Retzius-type cells in the domestic pig provide an opportunity to study their neuronal connections and the possible role of reelin in plasticity and regeneration of neocortex
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