On tests of activation map dimension for fMRI-based studies of learning

Methodology for linking fMRI BOLD signal distributional changes associated with paradigm-related learning remains needed. Herein we consider settings where task related activation may be present before and after learning, yet the distribution of activated voxels changes. For context, consider the study of a motor learning task performed in scanner twice prior to and after a training session compared with a control motor task of equal difficulty occurring twice but without training. Current methodology would likely use random effect statistical parametric mapping to test the interaction of training on task. However, this approach suffers from considering estimated voxel-level activation or change in activation in isolation. In contrast, learning may evidence itself in changes in activation distribution , i.e. the distribution of intensities of BOLD response to the paradigm. The use of the analyses of lower dimensional subspaces of fMRI task-based activation maps provides our starting framework for such analysis. This manuscript investigates tests of dimension for the study of learning, particularly motor learning. The proposed methods consider the distribution of activation maps and tests the dimension of activation distribution between a trained and untrained tasks. If the BOLD signal is identical between the tasks (up to noise) the activation distribution should be one dimensional. The proposed analysis formally tests dimension in this setting. The methodology is formally developed and evaluated via simulation.Our investigation includes a large scale simulation study of brain activation maps, motivated by a study of motor learning in healthy adults. Our simulation results demon- strate that the study of linear dimension reduction using the singular value decompo- sition in a framework similar to Zarahn (2002) is able to capture specific instances of learning effects. The method is illustrated on the motivating data set

Wideband tunable perfect absorption of graphene plasmons via attenuated total reflection in Otto prism configuration

A strategy is proposed to achieve wideband tunable perfect plasmonic absorption in graphene nanoribbons by employing attenuated total refraction (ATR) in Otto prism configuration. In this configuration, the Otto prism with a deep-subwavelength dielectric spacer is used to generate tunneling evanescent waves to excite localized plasmons in graphene nanoribbons. The influence of the configuration parameters on the absorption spectra of graphene plasmons is studied systematically, and the key finding is that perfect absorption can be achieved by actively controlling the incident angle of light under ATR conditions, which provides an effective degree of freedom to tune the absorption properties of graphene plasmons. Based on this result, it is further demonstrated that by simultaneously tuning the incident angle and the graphene Fermi energy, the tunable absorption waveband can be significantly enlarged, which is about 3 times wider than the conventional cavity-enhanced configuration. Our proposed strategy to achieve wideband, tunable graphene plasmons could be useful in various infrared plasmonic devices

Genetic variability and functional implication of the long control region in HPV-16 variants in Southwest China

<div><p>HPV-16 long control region (LCR) has been shown to be the most variable region of the HPV-16 genome and may play important roles in viral persistence and the development of cervical cancer. This study aimed to assess the risk of HPV-16 LCR variants for cervical cancer in women of Southwest China. 2146 cervical scrapings of volunteer outpatients and 74 cervical cancer tissues were screened.14 entire HPV-16 LCRs from asymptomatic carriers and 34 entire HPV-16 LCRs from cervical cancer patients were successfully amplified and sequenced to align to others described. 58 different point mutations were detected in 54 nucleotide sites of HPV-16 LCR. G7193T and G7521A variants, accounting for 100% of the infections, were predicted to locate at the binding site for FOXA1 and SOX9, respectively. A7730C variant which showed a high mutation frequency in cervical cancer was predicted to be a binding site for the cellular transcription factor PHOX2A. In addition, phylogenetic analysis displayed a high prevalence of A lineage in HPV-16 LCR in this Southwest China population. This study may help understanding of the intrinsic geographical relatedness and the correlations between LCR mutations and the development of carcinogenic lesions in Southwest China population. And it provides useful data for the further study of the biological function of HPV-16 LCR variants.</p></div

The potential binding sites of cellular transcription factors within HPV-16 LCR.

<p>The JASPAR database was used to investigate the potential binding sites within HPV-16 LCR. The proposed binding sites for transcription factors were separately marked on the bold nucleotide mutation sites.</p

HPV genotype distribution of outpatients and cervical cancer sufferers.

<p>HPV genotyping was performed using a nested PCR assay. The distribution of HPV genotype among HPV-positive outpatients and cervical cancer sufferers were shown.</p

Phylogenetic tree of the HPV-16 variants based on LCR sequences.

<p>The Neighbor-Joining method and the Kimura 2-Parameter model were used to construct the phylogenetic tree by MEGA package 7.0. The standard sequences included NC_001526.3, K02718 (A1), AF536179 (A2), HQ644236 (A3), AF534061 (A4), AF536180 (B1), HQ644298 (B2), AF472509 (C), HQ644257 (D1), HQ644270 (D2) and AF402678 (D3). The lineage to which each accession number belongs was shown in a parenthesis. Numbers closest to the branch points are bootstrap values (1,000 replicates). Values lower than 50% are not shown.</p

Nucleotide variations of HPV-16 LCR and the proposed binding sites for transcription factors.

<p>Nucleotide variations of HPV-16 LCR and the proposed binding sites for transcription factors.</p

Primer pairs designed for complete LCR amplification of HPV-16.

<p>Primer pairs designed for complete LCR amplification of HPV-16.</p