1,068 research outputs found
Criticality and isostaticity in fiber networks
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 , implying a breakdown of continuum
elasticity in this simple mechanical system on length scales less than .Comment: 6 pages, 5 figure
New Genetic Insights from Autoimmune Thyroid Disease
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
WISHEâMoisture Mode in an Aquaplanet Simulation
This study aims to understand the nature of the tropical intraseasonal oscillations (ISOs) in an aquaplanet simulation performed using Geophysical Fluid Dynamics Laboratoryâs AM2.1 with a uniform sea surface temperature within the deep tropics. The simulated ISO resembles the observed MaddenâJulian Oscillation in that the spectral peak in precipitation appears at zonal wave number 1 and a period of ~60Â 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 variablesâsurface wind stress, longwave radiative heating, and surface evaporationâwith their zonal means from the control simulation or by suppressing freeâtropospheric moisture variation. Results of the mechanism denial experiments show that the simulated ISO disappears when the interactive surface evaporation is disabled, suggesting that the windâinduced surface heat exchange (WISHE) mechanism is essential to the simulated ISO. Longwave cloudâradiation feedbacks and moistureâconvection feedbacks affect horizontal scale and phase speed of the simulated ISO, respectively. Our results strongly suggest that the simulated ISO is the linear WISHEâmoisture mode of Fuchs and Raymond under horizontally uniform boundary conditions.Key PointsAn aquaplanet simulation exhibits a mode of planetaryâscale (wave number 1), eastward propagating intraseasonal variabilityMoist static energy budget and mechanism denial experiments suggest that this mode is the linear WISHEâmoisture mode of Fuchs and RaymondThe WISHE and longwave cloudâradiation 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
Novel Non-Toxic Xylene Substitute (SBO) for Histology
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
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
Realization of Quantum Spin Hall State in Monolayer 1T'-WTe2
A quantum spin Hall (QSH) insulator is a novel two-dimensional quantum state
of matter that features quantized Hall conductance in the absence of magnetic
field, resulting from topologically protected dissipationless edge states that
bridge the energy gap opened by band inversion and strong spin-orbit coupling.
By investigating electronic structure of epitaxially grown monolayer 1T'-WTe2
using angle-resolved photoemission (ARPES) and first principle calculations, we
observe clear signatures of the topological band inversion and the band gap
opening, which are the hallmarks of a QSH state. Scanning tunneling microscopy
measurements further confirm the correct crystal structure and the existence of
a bulk band gap, and provide evidence for a modified electronic structure near
the edge that is consistent with the expectations for a QSH insulator. Our
results establish monolayer 1T'-WTe2 as a new class of QSH insulator with large
band gap in a robust two-dimensional materials family of transition metal
dichalcogenides (TMDCs).Comment: 19 pages, 4 figures; includes Supplemental Material (11 pages, 7
figures
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