1,491 research outputs found

    The simulation of action disorganisation in complex activities of daily living

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    Action selection in everyday goal-directed tasks of moderate complexity is known to be subject to breakdown following extensive frontal brain injury. A model of action selection in such tasks is presented and used to explore three hypotheses concerning the origins of action disorganisation: that it is a consequence of reduced top-down excitation within a hierarchical action schema network coupled with increased bottom-up triggering of schemas from environmental sources, that it is a more general disturbance of schema activation modelled by excessive noise in the schema network, and that it results from a general disturbance of the triggering of schemas by object representations. Results suggest that the action disorganisation syndrome is best accounted for by a general disturbance to schema activation, while altering the balance between top-down and bottom-up activation provides an account of a related disorder - utilisation behaviour. It is further suggested that ideational apraxia (which may result from lesions to left temporoparietal areas and which has similar behavioural consequences to action disorganisation syndrome on tasks of moderate complexity) is a consequence of a generalised disturbance of the triggering of schemas by object representations. Several predictions regarding differences between action disorganisation syndrome and ideational apraxia that follow from this interpretation are detailed

    Macrophage Subset Sensitivity to Endotoxin Tolerisation by Porphyromonas gingivalis

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    Macrophages (MΦs) determine oral mucosal responses; mediating tolerance to commensal microbes and food whilst maintaining the capacity to activate immune defences to pathogens. MΦ responses are determined by both differentiation and activation stimuli, giving rise to two distinct subsets; pro-inflammatory M1- and anti-inflammatory/regulatory M2- MΦs. M2-like subsets predominate tolerance induction whereas M1 MΦs predominate in inflammatory pathologies, mediating destructive inflammatory mechanisms, such as those in chronic P.gingivalis (PG) periodontal infection. MΦ responses can be suppressed to benefit either the host or the pathogen. Chronic stimulation by bacterial pathogen associated molecular patterns (PAMPs), such as LPS, is well established to induce tolerance. The aim of this study was to investigate the susceptibility of MΦ subsets to suppression by P. gingivalis. CD14hi and CD14lo M1- and M2-like MΦs were generated in vitro from the THP-1 monocyte cell line by differentiation with PMA and vitamin D3, respectively. MΦ subsets were pre-treated with heat-killed PG (HKPG) and PG-LPS prior to stimulation by bacterial PAMPs. Modulation of inflammation was measured by TNFα, IL-1β, IL-6, IL-10 ELISA and NFκB activation by reporter gene assay. HKPG and PG-LPS differentially suppress PAMP-induced TNFα, IL-6 and IL-10 but fail to suppress IL-1β expression in M1 and M2 MΦs. In addition, P.gingivalis suppressed NFκB activation in CD14lo and CD14hi M2 regulatory MΦs and CD14lo M1 MΦs whereas CD14hi M1 pro-inflammatory MΦs were refractory to suppression. In conclusion, P.gingivalis selectively tolerises regulatory M2 MΦs with little effect on pro-inflammatory CD14hi M1 MΦs; differential suppression facilitating immunopathology at the expense of immunity

    Quantum Tricritical Points in NbFe2_2

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    Quantum critical points (QCPs) emerge when a 2nd order phase transition is suppressed to zero temperature. In metals the quantum fluctuations at such a QCP can give rise to new phases including unconventional superconductivity. Whereas antiferromagnetic QCPs have been studied in considerable detail ferromagnetic (FM) QCPs are much harder to access. In almost all metals FM QCPs are avoided through either a change to 1st order transitions or through an intervening spin-density-wave (SDW) phase. Here, we study the prototype of the second case, NbFe2_2. We demonstrate that the phase diagram can be modelled using a two-order-parameter theory in which the putative FM QCP is buried within a SDW phase. We establish the presence of quantum tricritical points (QTCPs) at which both the uniform and finite qq susceptibility diverge. The universal nature of our model suggests that such QTCPs arise naturally from the interplay between SDW and FM order and exist generally near a buried FM QCP of this type. Our results promote NbFe2_2 as the first example of a QTCP, which has been proposed as a key concept in a range of narrow-band metals, including the prominent heavy-fermion compound YbRh2_2Si2_2.Comment: 21 pages including S

    The Target Selective Neural Response — Similarity, Ambiguity, and Learning Effects

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    A network of frontal and parietal brain regions is commonly recruited during tasks that require the deliberate ‘top-down’ control of thought and action. Previously, using simple target detection, we have demonstrated that within this frontoparietal network, the right ventrolateral prefrontal cortex (VLPFC) in particular is sensitive to the presentation of target objects. Here, we use a range of target/non-target morphs to plot the target selective response within distinct frontoparietal sub-regions in greater detail. The increased resolution allows us to examine the extent to which different cognitive factors can predict the blood oxygenation level dependent (BOLD) response to targets. Our results reveal that both probability of positive identification (similarity to target) and proximity to the 50% decision boundary (ambiguity) are significant predictors of BOLD signal change, particularly in the right VLPFC. Furthermore, the profile of target related signal change is not static, with the degree of selectivity increasing as the task becomes familiar. These findings demonstrate that frontoparietal sub-regions are recruited under increased cognitive demand and that when recruited, they adapt, using both fast and slow mechanisms, to selectively respond to those items that are of the most relevance to current intentions

    Island extinctions: processes, patterns, and potential for ecosystem restoration

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    Extinctions have altered island ecosystems throughout the late Quaternary. Here, we review the main historic drivers of extinctions on islands, patterns in extinction chronologies between islands, and the potential for restoring ecosystems through reintroducing extirpated species. While some extinctions have been caused by climatic and environmental change, most have been caused by anthropogenic impacts. We propose a general model to describe patterns in these anthropogenic island extinctions. Hunting, habitat loss and the introduction of invasive predators accompanied prehistoric settlement and caused declines of endemic island species. Later settlement by European colonists brought further land development, a different suite of predators and new drivers, leading to more extinctions. Extinctions alter ecological networks, causing ripple effects for islands through the loss of ecosystem processes, functions and interactions between species. Reintroduction of extirpated species can help restore ecosystem function and processes, and can be guided by palaeoecology. However, reintroduction projects must also consider the cultural, social and economic needs of humans now inhabiting the islands and ensure resilience against future environmental and climate change
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