Objective: Both structural and functional brain connectivities are closely linked to white matter disease. We discuss several such links of potential interest to neurologists, neurosurgeons, radiologists, and non-clinical neuroscientists. Methods: Treatment of brains as genuine complex systems suggests major emphasis on the multi-scale nature of brain connectivity and dynamic behavior. Cross-scale interactions of local, regional, and global networks are apparently responsible for much of EEG's oscillatory behaviors. Finite axon propagation speed, often assumed to be infinite in local network models, is central to our conceptual framework. Results: Myelin controls axon speed, and the synchrony of impulse traffic between distant cortical regions appears to be critical for optimal mental performance and learning. Several experiments suggest that axon conduction speed is plastic, thereby altering the regional and global white matter connections that facilitate binding of remote local networks. Conclusions: Combined EEG and high resolution EEG can provide distinct multi-scale estimates of functional connectivity in both healthy and diseased brains with measures like frequency and phase spectra, covariance, and coherence. Significance: White matter disease may profoundly disrupt normal EEG coherence patterns, but currently these kinds of studies are rare in scientific labs and essentially missing from clinical environments.

The spatial statistics of scalp electroencephalogram (EEG) are usually presented as coherence in individual frequency bands. These coherences result both from correlations among neocortical sources and volume conduction through the tissues of the head. The scalp EEG is spatially low-pass filtered by the poorly conducting skull, introducing artificial correlation between the electrodes. A four concentric spheres (brain, CSF, skull, and scalp) model of the head and stochastic field theory are used here to derive an analytic estimate of the coherence at scalp electrodes due to volume conduction of uncorrelated source activity, predicting that electrodes within 10-12 cm can appear correlated. The surface Laplacian estimate of cortical surface potentials spatially bandpass filters the scalp potentials reducing this artificial coherence due to volume conduction. Examination of EEG data confirms that the coherence estimates from raw scalp potentials and Laplacians are sensitive to different spatial bandwidths and should be used in parallel in studies of neocortical dynamic function.

Object

A novel method of estimating metabolite T1 relaxation times using MR spectroscopic imaging (MRSI) is proposed. As opposed to conventional single-voxel metabolite T1 estimation methods, this method investigates regional and gray matter (GM)/white matter (WM) differences in metabolite T1 by taking advantage of the spatial distribution information provided by MRSI.

Material and methods

The method, validated by Monte Carlo studies, involves a voxel averaging to preserve the GM/WM distribution, a non-linear least squares fit of the metabolite T1 and an estimation of its standard error by bootstrapping. It was applied in vivo to estimate the T1 of N-acetyl compounds (NAA), choline, creatine and myo-inositol in eight normal volunteers, at 1.5 T, using a short echo time 2D-MRSI slice located above the ventricles.

Results

WM-T 1,NAA was significantly (P < 0.05) longer in anterior regions compared to posterior regions of the brain. The anterior region showed a trend of a longer WM T1 compared to GM for NAA, creatine and myo-Inositol. Lastly, accounting for the bootstrapped standard error estimate in a group mean T1 calculation yielded a more accurate T1 estimation.

Conclusion

The method successfully measured in vivo metabolite T1 using MRSI and can now be applied to diseased brain.

Two different methods to improve the spatial resolution of EEG are discussed: the surface Laplacian (e.g., current source density) and cortical imaging (e.g., spatial deconvolution). The former methods tend to be independent of head volume conductor model, whereas the latter methods are more model-dependent. Computer simulation of scalp potentials due to either a few isolated sources or 4200 distributed cortical sources and studies of actual EEG data both indicate that the two methods provide similar estimates of cortical potential distribution. Typical correlation coefficients between either spline-Laplacian or cortical image and simulated (calculated) cortical potential are in the 0.8-0.95 range, depending partly on CSF thickness. By contrast, correlation coefficients between simulated scalp and cortical potential are in the 0.4-0.5 range, suggesting that high resolution methods provide much better estimates of cortical potential than is obtained with conventional EEG. The two methods are also applied to steady-state visually evoked potentials and spontaneous EEG. Correlation coefficients obtained from real EEG data are in the same general ranges as correlations obtained from simulations. The new high resolution methods can provide a dramatic increase in the information content of EEG and appear to have widespread application in both clinical and cognitive studies.

Okra germplasm collected from different locations around the world were screened at AVRDC(The World Vegetable Center) in 2011 and 2012 to identify germplasm resistant to the melon aphid (Aphis gossypii) for use in sub-Saharan Africa. A total of 260 okra accessions and varieties were screened (150 at AVRDC Taiwan and 110 at AVRDC Cameroon), which included four varieties commercially available in Cameroon. The experiments were conducted under natural infestation in Shanhua, Taiwan, and at Yaoundé, Cameroon. Since the preliminary screening trials were conducted in Taiwan and Cameroon, the aphid populations in these two countries were compared. A total of 60 insects was used for cytochrome c oxidase I (COI) gene sequencing and phylogenetic analysis. The nucleotide sequences of all the populations showed 100 % similarity and the phylogenetic analysis confirmed the genetic similarity of A. gossypii in Taiwan and Cameroon. Results of the screening trials showed that three accessions (VI033805, VI036213 and VI051114) were resistant to A. gossypii. The basis of resistance of the three okra accessions was elucidated by studying their biochemical and biophysical properties. There was no significant difference between the susceptible and resistant okra accessions in terms of leaf tannins, free amino acids, total sugars and total phenols. Only total nitrogen was significantly different between the susceptible and the two resistant okra accessions with the lowest aphid infestation (VI033805 and VI036213). Thus, higher leaf nitrogen content seems to favour the aphid infestation on okra. For physical parameters, there was no significant difference among the accessions in trichome density of bottom and middle leaves, and leaf toughness. However, trichome density in the younger leaves of resistant VI033805 was significantly higher than susceptible VI057245. Studies on settling behaviour showed that aphids did not discriminate between the susceptible and resistant okra accessions for oviposition and feeding 72 h after release.

Summary cis-regulatory changes play a central role in morphological divergence, yet the regulatory principles underlying emergence of human traits remain poorly understood. Here, we use epigenomic profiling from human and chimpanzee cranial neural crest cells to systematically and quantitatively annotate divergence of craniofacial cis-regulatory landscapes. Epigenomic divergence is often attributable to genetic variation within TF motifs at orthologous enhancers, with a novel motif being most predictive of activity biases. We explore properties of this cis-regulatory change, revealing the role of particular retroelements, uncovering broad clusters of species-biased enhancers near genes associated with human facial variation, and demonstrating that cis-regulatory divergence is linked to quantitative expression differences of crucial neural crest regulators. Our work provides a wealth of candidates for future evolutionary studies and demonstrates the value of "cellular anthropology," a strategy of using in-vitro-derived embryonic cell types to elucidate both fundamental and evolving mechanisms underlying morphological variation in higher primates.

Abstract Background Lymph node metastasis constitutes a key event in tumor progression. The molecular control of this process is poorly understood. Heparan sulfate is a linear polysaccharide consisting of unique sulfate-modified disaccharide repeats that allow the glycan to bind a variety of proteins, including chemokines. While some chemokines may drive lymphatic trafficking of tumor cells, the functional and genetic importance of heparan sulfate as a possible mediator of chemokine actions in lymphatic metastasis has not been reported. Results We applied a loss-of-function genetic approach employing lymphatic endothelial conditional mutations in heparan sulfate biosynthesis to study the effects on tumor-lymphatic trafficking and lymph node metastasis. Lymphatic endothelial deficiency in N-deacetylase/N-sulfotransferase-1 (Ndst1), a key enzyme involved in sulfating nascent heparan sulfate chains, resulted in altered lymph node metastasis in tumor-bearing gene targeted mice. This occurred in mice harboring either a pan-endothelial Ndst1 mutation or an inducible lymphatic-endothelial specific mutation in Ndst1. In addition to a marked reduction in tumor metastases to the regional lymph nodes in mutant mice, specific immuno-localization of CCL21, a heparin-binding chemokine known to regulate leukocyte and possibly tumor-cell traffic, showed a marked reduction in its ability to associate with tumor cells in mutant lymph nodes. In vitro modified chemotaxis studies targeting heparan sulfate biosynthesis in lymphatic endothelial cells revealed that heparan sulfate secreted by lymphatic endothelium is required for CCL21-dependent directional migration of murine as well as human lung carcinoma cells toward the targeted lymphatic endothelium. Lymphatic heparan sulfate was also required for binding of CCL21 to its receptor CCR7 on tumor cells as well as the activation of migration signaling pathways in tumor cells exposed to lymphatic conditioned medium. Finally, lymphatic cell-surface heparan sulfate facilitated receptor-dependent binding and concentration of CCL21 on the lymphatic endothelium, thereby serving as a mechanism to generate lymphatic chemokine gradients. Conclusions This work demonstrates the genetic importance of host lymphatic heparan sulfate in mediating chemokine dependent tumor-cell traffic in the lymphatic microenvironment. The impact on chemokine dependent lymphatic metastasis may guide novel therapeutic strategies.

The cotton aphid (Aphis gossypii) is one of the major pests of okra. Eleven okra varieties collected from farmers' fields in Cameroon and four aphid-resistant accessions from The World Vegetable Center (AVRDC, Asian Vegetable Research and Development Center) were evaluated from October 2012 to March 2013, and another seven aphid-resistant accessions from AVRDC were evaluated from March to July 2013 at AVRDC's Nkolbisson station, Yaoundé, Cameroon. Accessions selected from these trials were screened in an advanced confirmatory screening in autumn (October–December) 2013 in Shanhua, Taiwan. Results showed that none of the farmers' landraces were resistant to aphids. Two accessions (VI041210 and VI033824) with the lowest aphid populations had the highest trichome density. Analysis of various phytochemicals in selected okra accessions revealed that higher nitrogen and potassium levels made the okra accessions susceptible to aphids during the reproductive stage of the plants. Similarly, the total phenol content was lower in moderately resistant accessions during their reproductive stage. Aphid feeding induced an increase in phenols, and to a lesser extent, tannins. Accessions VI041210 and VI033824 could be incorporated into an integrated pest management strategy to enhance productivity of okra.

Background: Notch4 is a member of the Notch family of receptors that is primarily expressed in the vascular endothelial cells. Genetic deletion of Notch4 does not result in an overt phenotype in mice, thus the function of Notch4 remains poorly understood.