Cortical Surface Area and Cortical Thickness Demonstrate Differential Structural Asymmetry in Auditory-Related Areas of the Human Cortex

This investigation provides an analysis of structural asymmetries in 5 anatomically defined regions (Heschl's gyrus, HG; Heschl's sulcus, HS; planum temporale, PT; planum polare, PP; superior temporal gyrus, STG) within the human auditory-related cortex. Volumetric 3-dimensional T1-weighted magnetic resonance imaging scans were collected from 104 participants (52 males). Cortical volume (CV), cortical thickness (CT), and cortical surface area (CSA) were calculated based on individual scans of these anatomical traits. This investigation demonstrates a leftward asymmetry for CV and CSA that is observed in the HG, STG, and PT regions. As regards CT, we note a rightward asymmetry in the HG and HS. A correlation analysis of asymmetry indices between measurements for distinct regions of interest (ROIs) yields significant correlations between CT and CV in 4 of 5 ROIs (HG, HS, PT, and STG). Significant correlation values between CSA and CV are observed for all 5 ROIs. The findings suggest that auditory-related cortical areas demonstrate larger leftward asymmetry with respect to the CSA, while a clear rightward asymmetry with respect to CT is salient in both the primary and the secondary auditory cortex only. In addition, we propose that CV is not an ideal neuromarker for anatomical measurements. CT and CSA should be considered independent traits of anatomical asymmetries in the auditory-related corte

Tuning the mobility of a driven Bose-Einstein condensate via diabatic Floquet bands

We study the response of ultracold atoms to a weak force in the presence of a temporally strongly modulated optical lattice potential. It is experimentally demonstrated that the strong ac-driving allows for a tailoring of the mobility of a dilute atomic Bose-Einstein condensate with the atoms moving ballistically either along or against the direction of the applied force. Our results are in agreement with a theoretical analysis of the Floquet spectrum of a model system, thus revealing the existence of diabatic Floquet bands in the atom's band spectra and highlighting their role in the non-equilibrium transport of the atoms

Quantum creep and quantum creep transitions in 1D sine-Gordan chains

Discrete sine-Gordon (SG) chains are studied with path-integral molecular dynamics. Chains commensurate with the substrate show the transition from collective quantum creep to pinning at bead masses slightly larger than those predicted from the continuous SG model. Within the creep regime, a field-driven transition from creep to complete depinning is identified. The effects of disorder in the external potential on the chain's dynamics depend on the potential's roughness exponent $H$, i.e., quantum and classical fluctuations affect the current self-correlation functions differently for $H = 1/2$.Comment: 4 pages, 3 figure

Targeting High Mobility Group Box 1 in Subarachnoid Hemorrhage: A Systematic Review

Aneurysmal subarachnoid hemorrhage (aSAH) is a complex and potentially deadly disease. Neurosurgical clipping or endovascular coiling can successfully obliterate ruptured aneurysms in almost every case. However, despite successful interventions, the clinical outcomes of aSAH patients are often poor. The reasons for poor outcomes are numerous, including cerebral vasospasm (CVS), post-hemorrhagic hydrocephalus, systemic infections and delayed cerebral ischemia. Although CVS with subsequent cerebral ischemia is one of the main contributors to brain damage after aSAH, little is known about the underlying molecular mechanisms of brain damage. This review emphasizes the importance of pharmacological interventions targeting high mobility group box 1 (HMGB1)-mediated brain damage after subarachnoid hemorrhage (SAH) and CVS. We searched Pubmed, Ovid medline and Scopus for “subarachnoid hemorrhage” in combination with “HMGB1”. Based on these criteria, a total of 31 articles were retrieved. After excluding duplicates and selecting the relevant references from the retrieved articles, eight publications were selected for the review of the pharmacological interventions targeting HMGB1 in SAH. Damaged central nervous system cells release damage-associated molecular pattern molecules (DAMPs) that are important for initiating, driving and sustaining the inflammatory response following an aSAH. The discussed evidence suggested that HMGB1, an important DAMP, contributes to brain damage during early brain injury and also to the development of CVS during the late phase. Different pharmacological interventions employing natural compounds with HMGB1-antagonizing activity, antibody targeting of HMGB1 or scavenging HMGB1 by soluble receptors for advanced glycation end products (sRAGE), have been shown to dampen the inflammation mediated brain damage and protect against CVS. The experimental data suggest that HMGB1 inhibition is a promising strategy to reduce aSAH-related brain damage and CVS. Clinical studies are needed to validate these findings that may lead to the development of potential treatment options that are much needed in aSAH

Targeting High Mobility Group Box 1 in Subarachnoid Hemorrhage: A Systematic Review

Aneurysmal subarachnoid hemorrhage (aSAH) is a complex and potentially deadly disease. Neurosurgical clipping or endovascular coiling can successfully obliterate ruptured aneurysms in almost every case. However, despite successful interventions, the clinical outcomes of aSAH patients are often poor. The reasons for poor outcomes are numerous, including cerebral vasospasm (CVS), post-hemorrhagic hydrocephalus, systemic infections and delayed cerebral ischemia. Although CVS with subsequent cerebral ischemia is one of the main contributors to brain damage after aSAH, little is known about the underlying molecular mechanisms of brain damage. This review emphasizes the importance of pharmacological interventions targeting high mobility group box 1 (HMGB1)-mediated brain damage after subarachnoid hemorrhage (SAH) and CVS. We searched Pubmed, Ovid medline and Scopus for “subarachnoid hemorrhage” in combination with “HMGB1”. Based on these criteria, a total of 31 articles were retrieved. After excluding duplicates and selecting the relevant references from the retrieved articles, eight publications were selected for the review of the pharmacological interventions targeting HMGB1 in SAH. Damaged central nervous system cells release damage-associated molecular pattern molecules (DAMPs) that are important for initiating, driving and sustaining the inflammatory response following an aSAH. The discussed evidence suggested that HMGB1, an important DAMP, contributes to brain damage during early brain injury and also to the development of CVS during the late phase. Different pharmacological interventions employing natural compounds with HMGB1-antagonizing activity, antibody targeting of HMGB1 or scavenging HMGB1 by soluble receptors for advanced glycation end products (sRAGE), have been shown to dampen the inflammation mediated brain damage and protect against CVS. The experimental data suggest that HMGB1 inhibition is a promising strategy to reduce aSAH-related brain damage and CVS. Clinical studies are needed to validate these findings that may lead to the development of potential treatment options that are much needed in aSAH

Stochastic kinetics of viral capsid assembly based on detailed protein structures

We present a generic computational framework for the simulation of viral capsid assembly which is quantitative and specific. Starting from PDB files containing atomic coordinates, the algorithm builds a coarse grained description of protein oligomers based on graph rigidity. These reduced protein descriptions are used in an extended Gillespie algorithm to investigate the stochastic kinetics of the assembly process. The association rates are obtained from a diffusive Smoluchowski equation for rapid coagulation, modified to account for water shielding and protein structure. The dissociation rates are derived by interpreting the splitting of oligomers as a process of graph partitioning akin to the escape from a multidimensional well. This modular framework is quantitative yet computationally tractable, with a small number of physically motivated parameters. The methodology is illustrated using two different viruses which are shown to follow quantitatively different assembly pathways. We also show how in this model the quasi-stationary kinetics of assembly can be described as a Markovian cascading process in which only a few intermediates and a small proportion of pathways are present. The observed pathways and intermediates can be related a posteriori to structural and energetic properties of the capsid oligomers

Developmental dyscalculia: a dysconnection syndrome?

Numerical understanding is important for everyday life. For children with developmental dyscalculia (DD), numbers and magnitudes present profound problems which are thought to be based upon neuronal impairments of key regions for numerical understanding. The aim of the present study was to investigate possible differences in white matter fibre integrity between children with DD and controls using diffusion tensor imaging. White matter integrity and behavioural measures were evaluated in 15 children with developmental dyscalculia aged around 10years and 15 matched controls. The main finding, obtained by a whole brain group comparison, revealed reduced fractional anisotropy in the superior longitudinal fasciculus in children with developmental dyscalculia. In addition, a region of interest analysis exhibited prominent deficits in fibres of the superior longitudinal fasciculus adjacent to the intraparietal sulcus, which is thought to be the core region for number processing. To conclude, our results outline deficient fibre projection between parietal, temporal and frontal regions in children with developmental dyscalculia, and therefore raise the question of whether dyscalculia can be seen as a dysconnection syndrome. Since the superior longitudinal fasciculus is involved in the integration and control of distributed brain processes, the present results highlight the importance of considering broader domain-general mechanisms in the diagnosis and therapy of dyscalculia

Gliding dislocations in a driven vortex lattice

The dynamics of dislocations in a two-dimensional vortex lattice is studied in the presence of a pinning potential and a transport current. In a vortex lattice drifting with velocity $v$ a glide velocity $V_d$ of the dislocation with respect to the vortex lattice is found to decay like $V_d \sim v^{-4}$ for large drive. From this result the velocity for the crossover between a regime of coherent elastic motion and a regime of incoherent plastic motion of vortices is estimated.Comment: 4 pages Revte