The Effect of Resistivity on the Nonlinear Stage of the Magnetorotational Instability in Accretion Disks

We present three-dimensional magnetohydrodynamic simulations of the nonlinear evolution of the magnetorotational instability (MRI) with a non-zero Ohmic resistivity. The properties of the saturated state depend on the initial magnetic field configuration. In simulations with an initial uniform vertical field, the MRI is able to support angular momentum transport even for large resistivities through the quasi-periodic generation of axisymmetric radial channel solutions rather than through the maintenance of anisotropic turbulence. Simulations with zero net flux show that the angular momentum transport and the amplitude of magnetic energy after saturation are significantly reduced by finite resistivity, even at levels where the linear modes are only slightly affected. This occurs at magnetic Reynolds numbers expected in low, cool states of dwarf novae, these results suggest that finite resistivity may account for the low and high angular momentum transport rates inferred for these systems.Comment: 8 figures, accepted for publication in Ap

Electrical Modification of Combustion and the Affect of Electrode Geometry on the Field Produced

There has been extensive work to show how electric fields can influence combustion. However, many different set ups are used. This work shows how different set ups produce different field strengths and that the field is not always uniformly distributed. The field strength is modelled using Ansys Maxwell. The type of material used is discussed and the set up of apparatus. It is recommended to use parallel plates for experimentation. Parallel plates produce the most uniform field this allow's it's influence to be directly investigated and related to the field strength

USING KINETIC ISOMETRIC MID-THIGH PULL VARIABLES TO PREDICT D-I MALE SPRINTERS’ 60M PERFORMANCE

The purpose of the study was to determine the relationship of isometric mid-thigh pull kinetic variables including: peak force (PF), instantaneous force at 50, 90, 200 and 250 milliseconds (F@50, 90, 200 and 250 ms) rate of force development (RFD@ 50, 90, 200 and 250 ms) and impulse at 50, 90, 200, and 250 ms (IP @ 50, 90, 200 and 250 ms) to college male sprinters’ 60 m running performance. Eleven NCAA Division I male sprinters participated in the study that included two testing sessions. The first session included sprint testing and the second session included isometric mid-thigh pull strength assessment. The results from current study indicated that explosive force production variables (F@ 50 ms, RFD @ 50 and 90 ms, IP @ 90 and 200 ms) showed strong correlations with 60 m running time and maximal running velocity; while the MPF was not related to sprint variables

SMAD transcription factors are altered in cell models of HD and regulate HTT expression

Transcriptional dysregulation is observable in multiple animal and cell models of Huntington's disease, as well as in human blood and post-mortem caudate. This contributes to HD pathogenesis, although the exact mechanism by which this occurs is unknown. We therefore utilised a dynamic model in order to determine the differential effect of growth factor stimulation on gene expression, to highlight potential alterations in kinase signalling pathways that may be in part responsible for the transcriptional dysregulation observed in HD, and which may reveal new therapeutic targets. We demonstrate that cells expressing mutant huntingtin have a dysregulated transcriptional response to epidermal growth factor stimulation, and identify the transforming growth factor-beta pathway as a novel signalling pathway of interest that may regulate the expression of the Huntingtin (HTT) gene itself. The dysregulation of HTT expression may contribute to the altered transcriptional phenotype observed in HD

RNA-Seq of Huntington's disease patient myeloid cells reveals innate transcriptional dysregulation associated with proinflammatory pathway activation

Innate immune activation beyond the central nervous system is emerging as a vital component of the pathogenesis of neurodegeneration. Huntington’s disease (HD) is a fatal neurodegenerative disorder caused by a CAG repeat expansion in the huntingtin gene. The systemic innate immune system is thought to act as a modifier of disease progression; however, the molecular mechanisms remain only partially understood. Here we use RNA-sequencing to perform whole transcriptome analysis of primary monocytes from thirty manifest HD patients and thirty-three control subjects, cultured with and without a proinflammatory stimulus. In contrast with previous studies that have required stimulation to elicit phenotypic abnormalities, we demonstrate significant transcriptional differences in HD monocytes in their basal, unstimulated state. This includes previously undetected increased resting expression of genes encoding numerous proinflammatory cytokines, such as IL6. Further pathway analysis revealed widespread resting enrichment of proinflammatory functional gene sets, while upstream regulator analysis coupled with Western blotting suggests that abnormal basal activation of the NFOEB pathway plays a key role in mediating these transcriptional changes. That HD myeloid cells have a proinflammatory phenotype in the absence of stimulation is consistent with a priming effect of mutant huntingtin, whereby basal dysfunction leads to an exaggerated inflammatory response once a stimulus is encountered. These data advance our understanding of mutant huntingtin pathogenesis, establish resting myeloid cells as a key source of HD immune dysfunction, and further demonstrate the importance of systemic immunity in the potential treatment of HD and the wider study of neurodegeneration

A mathematical model for top-shelf vertigo: the role of sedimenting otoconia in BPPV

Benign Paroxysmal Positional Vertigo (BPPV) is a mechanical disorder of the vestibular system in which calcite particles called otoconia interfere with the mechanical functioning of the fluid-filled semicircular canals normally used to sense rotation. Using hydrodynamic models, we examine the two mechanisms proposed by the medical community for BPPV: cupulolithiasis, in which otoconia attach directly to the cupula (a sensory membrane), and canalithiasis, in which otoconia settle through the canals and exert a fluid pressure across the cupula. We utilize known hydrodynamic calculations and make reasonable geometric and physical approximations to derive an expression for the transcupular pressure $\Delta P_c$ exerted by a settling solid particle in canalithiasis. By tracking settling otoconia in a two-dimensional model geometry, the cupular volume displacement and associated eye response (nystagmus) can be calculated quantitatively. Several important features emerge: 1) A pressure amplification occurs as otoconia enter a narrowing duct; 2) An average-sized otoconium requires approximately five seconds to settle through the wide ampulla, where $\Delta P_c$ is not amplified, which suggests a mechanism for the observed latency of BPPV; and 3) An average-sized otoconium beginning below the center of the cupula can cause a volumetric cupular displacement on the order of 30 pL, with nystagmus of order $2^\circ$/s, which is approximately the threshold for sensation. Larger cupular volume displacement and nystagmus could result from larger and/or multiple otoconia.Comment: 15 pages, 5 Figures updated, to be published in J. Biomechanic