Investigations of attentional processing in parietal and occipital human cortical regions with magnetoencephalography

Attention defines our mental ability to select and respond to stimuli, internal or external, on the basis of behavioural goals in the presence of competing, behaviourally irrelevant, stimuli. The frontal and parietal cortices are generally agreed to be involved with attentional processing, in what is termed the 'fronto-parietal' network. The left parietal cortex has been seen as the site for temporal attentional processing, whereas the right parietal cortex has been seen as the site for spatial attentional processing. There is much debate about when the modulation of the primary visual cortex occurs, whether it is modulated in the feedforward sweep of processing or modulated by feedback projections from extrastriate and higher cortical areas. MEG and psychophysical measurements were used to look at spatially selective covert attention. Dual-task and cue-based paradigms were used. It was found that the posterior parietal cortex (PPC), in particular the SPL and IPL, was the main site of activation during these experiments, and that the left parietal lobe was activated more strongly than the right parietal lobe throughout. The levels of activation in both parietal and occipital areas were modulated in accordance with attentional demands. It is likely that spatially selective covert attention is dominated by the left parietal lobe, and that this takes the form of the proposed sensory-perceptual lateralization within the parietal lobes. Another form of lateralization is proposed, termed the motor-processing lateralization, the side of dominance being determined by handedness, being reversed in left- relative to right-handers. In terms of the modulation of the primary visual cortex, it was found that it is unlikely that V1 is modulated initially; rather the modulation takes the form of feedback from higher extrastriate and parietal areas. This fits with the idea of preattentive visual processing, a commonly accepted idea which, in itself, prevents the concept of initial modulation of V1.

Spatial patterns of FUS-immunoreactive neuronal cytoplasmic inclusions (NCI) in neuronal intermediate filament inclusion disease (NIFID)

Neuronal intermediate filament inclusion disease (NIFID), a rare form of frontotemporal lobar degeneration (FTLD), is characterized neuropathologically by focal atrophy of the frontal and temporal lobes, neuronal loss, gliosis, and neuronal cytoplasmic inclusions (NCI) containing epitopes of ubiquitin and neuronal intermediate filament (IF) proteins. Recently, the 'fused in sarcoma' (FUS) protein (encoded by the FUS gene) has been shown to be a component of the inclusions of NIFID. To further characterize FUS proteinopathy in NIFID, we studied the spatial patterns of the FUS-immunoreactive NCI in frontal and temporal cortex of 10 cases. In the cerebral cortex, sectors CA1/2 of the hippocampus, and the dentate gyrus (DG), the FUS-immunoreactive NCI were frequently clustered and the clusters were regularly distributed parallel to the tissue boundary. In a proportion of cortical gyri, cluster size of the NCI approximated to those of the columns of cells was associated with the cortico-cortical projections. There were no significant differences in the frequency of different types of spatial patterns with disease duration or disease stage. Clusters of NCI in the upper and lower cortex were significantly larger using FUS compared with phosphorylated, neurofilament heavy polypeptide (NEFH) or a-internexin (INA) immunohistochemistry (IHC). We concluded: (1) FUS-immunoreactive NCI exhibit similar spatial patterns to analogous inclusions in the tauopathies and synucleinopathies, (2) clusters of FUS-immunoreactive NCI are larger than those revealed by NEFH or ???, and (3) the spatial patterns of the FUS-immunoreactive NCI suggest the degeneration of the cortico-cortical projections in NIFID.

Growth of foliose lichens: a review

This review considers various aspects of the growth of foliose lichens including early growth and development, variation in radial growth rate (RaGR) of different species, growth to maturity, lobe growth variation, senescence and fragmentation, growth models, the influence of environmental variables, and the maintenance of thallus symmetry. The data suggest that a foliose lichen thallus is essentially a ‘colony’ in which the individual lobes exhibit a considerable degree of autonomy in their growth processes. During development, recognisable juvenile thalli are usually formed by 15 months to 4 years while most mature thalli exhibit RaGR between 1 and 5 mm yr-1. RaGR within a species is highly variable. The growth rate-size curve of a foliose lichen thallus may result from growth processes that take place at the tips of individual lobes together with size-related changes in the intensity of competition for space between the marginal lobes. Radial growth and growth in mass is influenced by climatic and microclimatic factors and also by substratum factors such as rock and bark texture, chemistry, and nutrient enrichment. Possible future research topics include: (1) measuring fast growing foliose species through life, (2) the three dimensional changes that occur during lobe growth, (3) the cellular changes that occur during regeneration, growth, and division of lobes, and (4) the distribution and allocation of the major lichen carbohydrates within lobes.

The dyslexia candidate locus on 2p12 is associated with general cognitive ability and white matter structure

Independent studies have shown that candidate genes for dyslexia and specific language impairment (SLI) impact upon reading/language-specific traits in the general population. To further explore the effect of disorder-associated genes on cognitive functions, we investigated whether they play a role in broader cognitive traits. We tested a panel of dyslexia and SLI genetic risk factors for association with two measures of general cognitive abilities, or IQ, (verbal and non-verbal) in the Avon Longitudinal Study of Parents and Children (ALSPAC) cohort (N>5,000). Only the MRPL19/C2ORF3 locus showed statistically significant association (minimum P = 0.00009) which was further supported by independent replications following analysis in four other cohorts. In addition, a fifth independent sample showed association between the MRPL19/C2ORF3 locus and white matter structure in the posterior part of the corpus callosum and cingulum, connecting large parts of the cortex in the parietal, occipital and temporal lobes. These findings suggest that this locus, originally identified as being associated with dyslexia, is likely to harbour genetic variants associated with general cognitive abilities by influencing white matter structure in localised neuronal regions.

A quantitative study of the pathological changes in the cortical white matter in variant Creutzfeld-Jakob disease (vCJD)

The objective of this study was to determine the degree of white matter pathology in the cerebral cortex in cases of variant Creutzfeldt-Jakob disease (vCJD) and to study the relationships between the white matter and grey matter pathologies. Hence, the pathological changes in cortical white matter were studied in individual gyri of the frontal, parietal, occipital, and temporal cortex in eleven cases of vCJD. Vacuolation (‘spongiform change’), deposition of the disease form of prion protein (PrPsc) in the form of discrete PrP deposits, and gliosis were observed in the white matter of virtually all cortical regions studied. Mean density of the vacuoles in the white matter was greater in the parietal lobe compared with the frontal, occipital, and temporal lobes but there were fewer glial cells in the occipital lobe compared with the other cortical regions. In the white matter of the frontal cortex, vacuole density was negatively correlated with the density of both glial cell nuclei and the PrP deposits. In addition, the densities of glial cells and PrP deposits were positively correlated in the frontal and parietal cortex. In the white matter of the frontal cortex and inferior temporal gyrus, there was a negative correlation between the densities of the vacuoles and the number of surviving neurons in laminae V/VI of the adjacent grey matter. In addition, in the frontal cortex, vacuole density in the white matter was negatively correlated with the density of the diffuse PrP deposits in laminae II/III and V/VI of the adjacent grey matter. The densities of PrP deposits in the white matter of the frontal cortex were positively correlated with the density of the diffuse PrP deposits in laminae II/III and V/V1 and with the number of surviving neurons in laminae V/V1. The data suggest that in the white matter in vCJD, gliosis is associated with the development of PrP deposits while the appearance of the vacuolation is a later development. In addition, neuronal loss and PrP deposition in the lower cortical laminae of the grey matter may be a consequence of axonal degeneration within the white matter.

A comparison of spatial patterns of TDP-43 cellular inclusions in familial and sporadic frontotemporal lobar degeneration with TDP-43 proteinopathy

Abnormal protein aggregates of transactive response (TAR) DNA-binding protein (TDP-43) in the form of neuronal cytoplasmic inclusions (NCI), oligodendroglial inclusions (GI), neuronal internuclear inclusions (NII), and dystrophic neurites (DN) are the pathological hallmark of frontotemporal lobar degeneration with TDP-43 proteinopathy (FTLD-TDP). To investigate the role of phosphorylated TDP-43 (pTDP-43) in neurodegeneration in FTLD-TDP, the spatial patterns of the pTDP-43-immunoreactive NCI, GI, NII, and DN were studied in frontal and temporal cortex in three groups of cases: (1) familial FTLD-TDP caused by progranulin (GRN) mutation, (2) a miscellaneous group of familial cases containing cases caused by valosin-containing protein (VCP) mutation, ubiquitin associated protein 1 (UBAP1) mutation, and cases not associated with currently known genes, and (3) sporadic FTLD-TDP. In a significant number of brain regions, the pTDP-43-immunoreactive inclusions developed in clusters and the clusters were distributed regularly parallel to the tissue boundary. The spatial patterns of the inclusions were similar to those revealed by a phosphorylation-independent anti-TDP-43 antibody. The spatial patterns and cluster sizes of the pTDP-43-immunoreactive inclusions were similar in GRN mutation cases, remaining familial cases, and in sporadic FTLD-TDP. Hence, pathological changes initiated by different genetic factors in familial cases and by unknown causes in sporadic FTLD-TDP appear to follow a parallel course resulting in very similar patterns of degeneration of frontal and temporal lobes.

Where do bright ideas occur in our brain? Meta-analytic evidence from neuroimaging studies of domain-specific creativity

Many studies have assessed the neural underpinnings of creativity, failing to find a clear anatomical localization. We aimed to provide evidence for a multi-componential neural system for creativity. We applied a general activation likelihood estimation (ALE) meta-analysis to 45 fMRI studies. Three individual ALE analyses were performed to assess creativity in different cognitive domains (Musical, Verbal, and Visuo-spatial). The general ALE revealed that creativity relies on clusters of activations in the bilateral occipital, parietal, frontal, and temporal lobes. The individual ALE revealed different maximal activation in different domains. Musical creativity yields activations in the bilateral medial frontal gyrus, in the left cingulate gyrus, middle frontal gyrus, and inferior parietal lobule and in the right postcentral and fusiform gyri. Verbal creativity yields activations mainly located in the left hemisphere, in the prefrontal cortex, middle and superior temporal gyri, inferior parietal lobule, postcentral and supramarginal gyri, middle occipital gyrus, and insula. The right inferior frontal gyrus and the lingual gyrus were also activated. Visuo-spatial creativity activates the right middle and inferior frontal gyri, the bilateral thalamus and the left precentral gyrus. This evidence suggests that creativity relies on multi-componential neural networks and that different creativity domains depend on different brain regions.

Probabilistic Approach to Design of Large Antenna Arrays

2000 Mathematics Subject Classification: 78A50

To move or not to move, that is the question! Body schema and non-action oriented body representations:an fMRI meta-analytic study

Many studies have attempted to identify the different cognitive components of body representation (BR). Due to methodological issues, the data reported in these studies are often confusing. Here we summarize the fMRI data from previous studies and explore the possibility of a neural segregation between BR supporting actions (body-schema, BS) or not (non-oriented-to-action-body-representation, NA). We performed a general activation likelihood estimation meta-analysis of 59 fMRI experiments and two individual meta-analyses to identify the neural substrates of different BR. Body processing involves a wide network of areas in occipital, parietal, frontal and temporal lobes. NA selectively activates the somatosensory primary cortex and the supramarginal gyrus. BS involves the primary motor area and the right extrastriate body area. Our data suggest that motor information and recognition of body parts are fundamental to build BS. Instead, sensory information and processing of the egocentric perspective are more important for NA. In conclusion, our results strongly support the idea that different and segregated neural substrates are involved in body representations orient or not to actions.

Survival in the pre-senile dementia frontotemporal lobar degeneration with TDP-43 proteinopathy:effects of genetic, demographic and neuropathological variables

Factors associated with survival were studied in 84 neuropathologically documented cases of the pre-senile dementia frontotemporal dementia lobar degeneration (FTLD) with transactive response (TAR) DNA-binding protein of 43 kDa (TDP-43) proteinopathy (FTLD-TDP). Kaplan-Meier survival analysis estimated mean survival as 7.9 years (range: 1-19 years, SD = 4.64). Familial and sporadic cases exhibited similar survival, including progranulin (GRN) gene mutation cases. No significant differences in survival were associated with sex, disease onset, Braak disease stage, or disease subtype, but higher survival was associated with lower post-mortem brain weight. Survival was significantly reduced in cases with associated motor neuron disease (FTLD-MND) but increased with Alzheimer's disease (AD) or hippocampal sclerosis (HS) co-morbidity. Cox regression analysis suggested that reduced survival was associated with increased densities of neuronal cytoplasmic inclusions (NCI) while increased survival was associated with greater densities of enlarged neurons (EN) in the frontal and temporal lobes. The data suggest that: (1) survival in FTLD-TDP is more prolonged than typical in pre-senile dementia but shorter than some clinical subtypes such as the semantic variant of primary progressive aphasia (svPPA), (2) MND co-morbidity predicts poor survival, and (3) NCI may develop early and EN later in the disease. The data have implications for both neuropathological characterization and subtyping of FTLD-TDP.

Optimizing the radiation pattern of smart antennas using genetic algorithms

This work is directed towards optimizing the radiation pattern of smart antennas using genetic algorithms. The structure of the smart antennas based on Space Division Multiple Access (SDMA) is proposed. It is composed of adaptive antennas, each of which has adjustable weight elements for amplitudes and phases of signals. The corresponding radiation pattern formula available for the utilization of numerical optimization techniques is deduced. Genetic algorithms are applied to search the best phase-amplitude weights or phase-only weights with which the optimal radiation pattern can be achieved. ^ One highlight of this work is the proposed optimal radiation pattern concept and its implementation by genetic algorithms. The results show that genetic algorithms are effective for the true Signal-Interference-Ratio (SIR) design of smart antennas. This means that not only nulls can be put in the directions of the interfering signals but also simultaneously main lobes can be formed in the directions of the desired signals. The optimal radiation pattern of a smart antenna possessing SDMA ability has been achieved. ^ The second highlight is on the weight search by genetic algorithms for the optimal radiation pattern design of antennas having more than one interfering signal. The regular criterion for determining which chromosome should be kept for the next step iteration is modified so as to improve the performance of the genetic algorithm iteration. The results show that the modified criterion can speed up and guarantee the iteration to be convergent. ^ In addition, the comparison between phase-amplitude perturbations and phase-only perturbations for the radiation pattern design of smart antennas are carried out. The effects of parameters used by the genetic algorithm on the optimal radiation pattern design are investigated. Valuable results are obtained. ^

Enhanced spectral compression in nonlinear optical fibres

We propose two new approaches to enhance the spectral compression process arising from nonlinear pulse propagation in an optical fibre. We numerically show that an additional sinusoidal temporal phase modulation of the pulse enables efficient reduction of the intensity level of side lobes in the spectrum. Another strategy is to select a regime of propagation in which normal group-velocity dispersion reshapes the initial stretched pulse to a near-Fourier-transform-limited rectangular waveform.

Enhanced nonlinear spectral compression in fiber by external sinusoidal phase modulation

We propose a new, simple approach to enhance the spectral compression process arising from nonlinear pulse propagation in an optical fiber. We numerically show that an additional sinusoidal temporal phase modulation of the pulse enables efficient reduction of the intensity level of the side lobes in the spectrum that are produced by the mismatch between the initial linear negative chirp of the pulse and the self-phase modulation-induced nonlinear positive chirp. Remarkable increase of both the extent of spectrum narrowing and the quality of the compressed spectrum is afforded by the proposed approach across a wide range of experimentally accessible parameters.

Enhanced nonlinear spectral compression in fibre by sinusoidal phase modulation

We propose a simple approach to enhance the spectral compression arising from nonlinear pulse propagation in a Kerr medium. We numerically show that an additional sinusoidal temporal phase modulation enables efficient reduction of the intensity level of spectral side lobes.

STRUCTURAL AND FUNCTIONAL CORRELATES OF EXERCISE VENTILATORY INEFFICIENCY IN CHRONIC OBSTRUCTIVE PULMONARY DISEASE PATIENTS WITH MILD-TO-MODERATE SPIROMETRIC ABNORMALITIES

Background: Individuals with chronic obstructive pulmonary disease (COPD) have higher than normal ventilatory equivalents for carbon dioxide (VE/VCO2) during exercise. There is growing evidence that emphysema on thoracic computed tomography (CT) scans is associated with poor exercise capacity in COPD patients with only mild-to-moderate airflow obstruction. We hypothesized that emphysema is an underlying cause of microvascular dysfunction and ventilatory inefficiency, which in turn contributes to reduced exercise capacity. We expected ventilatory inefficiency to be associated with a) the extent of emphysema; b) lower diffusing capacity for carbon monoxide; c) a reduced pulmonary blood flow response to exercise; and d) reduced exercise capacity. Methods: In a cross-sectional study, 19 subjects with mild-to-moderate COPD (mean ± SD FEV1= 82 ± 13% predicted, 12 GOLD grade 1) and 26 age-, sex-, and activity-matched controls underwent a ramp-incremental symptom-limited exercise test on a cycle ergometer. Ventilatory inefficiency was assessed by the minimum VE/VCO2 value (nadir). A subset of subjects also completed repeated constant work rate exercise bouts with non-invasive measurements of pulmonary blood flow. Emphysema was quantified as the percentage of attenuation areas below -950 Housefield Units on CT scans. An electronic scoresheet was used to keep track of emphysema sub-types. Results: COPD subjects typically had centrilobular emphysema (76.8 ± 10.1% of total emphysema) in the upper lobes (upper/lower lobe ratio= 0.82 ± 0.04). They had lower peak oxygen uptake (VO2), higher VE/VCO2 nadir and greater dyspnea scores than controls (p<0.05). Lower peak O2 and worse dyspnea were found in COPD subjects with VE/VCO2 nadirs ≥ 30. COPD subjects had blunted increases in pulmonary blood flow from rest to iso-VO2 exercise (p<0.05). Higher VE/VCO2 nadir in COPD subjects correlated with emphysema severity (r= 0.63), which in turn correlated with reduced lung diffusing capacity (r= -0.72) and blunted changes in pulmonary blood flow from rest to exercise (r= -0.69) (p<0.01). Conclusions: Ventilation “wasted” in emphysematous areas is associated with reduced exercise ventilatory efficiency in mild-to-moderate COPD. Exercise ventilatory inefficiency links structure (emphysema) and function (gas transfer) to a key clinical outcome (reduced exercise capacity) in COPD patients with modest spirometric abnormalities.