1,063 research outputs found

    Criticality and isostaticity in fiber networks

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    The rigidity of elastic networks depends sensitively on their internal connectivity and the nature of the interactions between constituents. Particles interacting via central forces undergo a zero-temperature rigidity-percolation transition near the isostatic threshold, where the constraints and internal degrees of freedom are equal in number. Fibrous networks, such as those that form the cellular cytoskeleton, become rigid at a lower threshold due to additional bending constraints. However, the degree to which bending governs network mechanics remains a subject of considerable debate. We study disordered fibrous networks with variable coordination number, both above and below the central-force isostatic point. This point controls a broad crossover from stretching- to bending-dominated elasticity. Strikingly, this crossover exhibits an anomalous power-law dependence of the shear modulus on both stretching and bending rigidities. At the central-force isostatic point---well above the rigidity threshold---we find divergent strain fluctuations together with a divergent correlation length Ο\xi, implying a breakdown of continuum elasticity in this simple mechanical system on length scales less than Ο\xi.Comment: 6 pages, 5 figure

    New Genetic Insights from Autoimmune Thyroid Disease

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    The autoimmune thyroid diseases (AITDs) (Graves' disease and Hashimoto's thyroiditis) are complex genetic diseases which most likely have more than 20 genes contributing to the clinical phenotypes. To date, the genes known to be contributing fall into two categories: immune regulatory genes (including HLA, CTLA4, PTPN22, CD40, CD25, and FCRL3) and thyroid-specific genes (TG and TSHR). However, none of these genes contribute more than a 4-fold increase in risk of developing one of these diseases, and none of the polymorphisms discovered is essential for disease development. Hence, it appears that a variety of different gene interactions can combine to cause the same clinical disease pattern, but the contributing genes may differ from patient to patient and from population to population. Furthermore, this possible mechanism leaves open the powerful influence of the environment and epigenetic modifications of gene expression. For the clinician, this means that genetic profiling of such patients is unlikely to be fruitful in the near future

    WISHE‐Moisture Mode in an Aquaplanet Simulation

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    This study aims to understand the nature of the tropical intraseasonal oscillations (ISOs) in an aquaplanet simulation performed using Geophysical Fluid Dynamics Laboratory’s AM2.1 with a uniform sea surface temperature within the deep tropics. The simulated ISO resembles the observed Madden‐Julian Oscillation in that the spectral peak in precipitation appears at zonal wave number 1 and a period of ~60 days. Vertically integrated moist static energy budget of the simulated ISO shows that enhanced latent heat flux to the east of anomalously active convection causes eastward propagation of the ISO mode, which is weakly opposed by horizontal moisture advection. A series of mechanism denial experiments are conducted either by homogenizing select variables—surface wind stress, longwave radiative heating, and surface evaporation—with their zonal means from the control simulation or by suppressing free‐tropospheric moisture variation. Results of the mechanism denial experiments show that the simulated ISO disappears when the interactive surface evaporation is disabled, suggesting that the wind‐induced surface heat exchange (WISHE) mechanism is essential to the simulated ISO. Longwave cloud‐radiation feedbacks and moisture‐convection feedbacks affect horizontal scale and phase speed of the simulated ISO, respectively. Our results strongly suggest that the simulated ISO is the linear WISHE‐moisture mode of Fuchs and Raymond under horizontally uniform boundary conditions.Key PointsAn aquaplanet simulation exhibits a mode of planetary‐scale (wave number 1), eastward propagating intraseasonal variabilityMoist static energy budget and mechanism denial experiments suggest that this mode is the linear WISHE‐moisture mode of Fuchs and RaymondThe WISHE and longwave cloud‐radiation feedbacks serve as scale selection mechanisms for the intraseasonal variabilityPeer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/146576/1/jame20767_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/146576/2/jame20767.pd

    Over-the-air Radiated Testing of Millimeter-Wave Beam-steerable Devices in a Cost-Effective Measurement Setup

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    Throughput Modeling and Validations for MIMO-OTA Testing with Arbitrary Multipath

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    Experimental Evaluation of User Influence on Test Zone Size in Multi-probe Anechoic Chamber Setups

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    An example of enhanced tephra deposition driven by topographically-induced atmospheric turbulence

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    Spatial variations in the thickness and grain-size characteristics of tephra fall deposits imply that tephra depositional processes cannot be fully captured by models of single-particle sedimentation from the base of the eruption plume. Here, we document a secondary thickness maximum in a ∌9.75 ka tephra fall deposit from ChaitĂ©n volcano, Chile (Cha1 eruption). This secondary thickness maximum is notably coarser-grained than documented historical examples, being dominated by medium-grained ash, and an origin via particle aggregation is therefore unlikely. In the region of secondary thickening, we propose that high levels of atmospheric turbulence accelerated particles held within the mid- to lower-troposphere (0 to ∌6 km) towards the ground surface. We suggest that this enhancement in vertical atmospheric mixing was driven by the breaking of lee waves, generated by winds passing over elevated topography beneath the eruption plume. Lower atmospheric circulation patterns may exert a significant control on the dispersal and deposition of tephra from eruption plumes across all spatial scales, particularly in areas of complex topography

    Novel Non-Toxic Xylene Substitute (SBO) for Histology

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    Xylene has been generally used as a clearing and deparaffinizing agent in histology. Because of the potential toxic and flammable nature of xylene, its substitutes have been introduced into some laboratories. In this study, we introduced a novel, non-toxic xylene substitute (SBO), which was  generated through a mixture of 86% of white oil No.2 and 14% of N-heptane. SBO had a high boiling point (188°C) and flash point (144°C) coupled with a scentless and decreased volatility. To compare the effectiveness of SBO and xylene in histology, a wide range of tissue samples from rats and human beings were processed in parallel in SBO and xylene, subjected to various staining procedures. Similar to the xylene-processed paraffin blocks, the SBO-processed counterparts were easy to section without any evidence of cell shrinkage. Assessment of the SBO-treated sections stained with hematoxylin-eosin revealed a good maintenance of cell morphology and structure, and a clear definition of the cytoplasm and the nucleus. Moreover, comparable good results were achieved between the SBO- and xylene-processed tissues in other histochemical and immunohistochemical stainings. Six-month clinical applications at one department of pathology supported the potentials of SBO as a xylene substitute. In conclusion, we suggest that SBO is a safe and efficient substitute of xylene and may probably replace xylene without losing valuable diagnostic information.Key words: SBO, clearing agent, xylene, histology, toxicit

    Associations of NINJ2 sequence variants with incident ischemic stroke in the Cohorts for Heart and Aging in Genomic Epidemiology (CHARGE) consortium

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    Background<p></p> Stroke, the leading neurologic cause of death and disability, has a substantial genetic component. We previously conducted a genome-wide association study (GWAS) in four prospective studies from the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) consortium and demonstrated that sequence variants near the NINJ2 gene are associated with incident ischemic stroke. Here, we sought to fine-map functional variants in the region and evaluate the contribution of rare variants to ischemic stroke risk.<p></p> Methods and Results<p></p> We sequenced 196 kb around NINJ2 on chromosome 12p13 among 3,986 European ancestry participants, including 475 ischemic stroke cases, from the Atherosclerosis Risk in Communities Study, Cardiovascular Health Study, and Framingham Heart Study. Meta-analyses of single-variant tests for 425 common variants (minor allele frequency [MAF] ≄ 1%) confirmed the original GWAS results and identified an independent intronic variant, rs34166160 (MAF = 0.012), most significantly associated with incident ischemic stroke (HR = 1.80, p = 0.0003). Aggregating 278 putatively-functional variants with MAF≀ 1% using count statistics, we observed a nominally statistically significant association, with the burden of rare NINJ2 variants contributing to decreased ischemic stroke incidence (HR = 0.81; p = 0.026).<p></p> Conclusion<p></p> Common and rare variants in the NINJ2 region were nominally associated with incident ischemic stroke among a subset of CHARGE participants. Allelic heterogeneity at this locus, caused by multiple rare, low frequency, and common variants with disparate effects on risk, may explain the difficulties in replicating the original GWAS results. Additional studies that take into account the complex allelic architecture at this locus are needed to confirm these findings
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