728 research outputs found
Thermally Induced Fluctuations Below the Onset of Rayleigh-B\'enard Convection
We report quantitative experimental results for the intensity of
noise-induced fluctuations below the critical temperature difference for Rayleigh-B\'enard convection. The structure factor of the fluctuating
convection rolls is consistent with the expected rotational invariance of the
system. In agreement with predictions based on stochastic hydrodynamic
equations, the fluctuation intensity is found to be proportional to
where . The
noise power necessary to explain the measurements agrees with the prediction
for thermal noise. (WAC95-1)Comment: 13 pages of text and 4 Figures in a tar-compressed and uuencoded file
(using uufiles package). Detailed instructions of unpacking are include
Spiral Defect Chaos in Large Aspect Ratio Rayleigh-Benard Convection
We report experiments on convection patterns in a cylindrical cell with a
large aspect ratio. The fluid had a Prandtl number of approximately 1. We
observed a chaotic pattern consisting of many rotating spirals and other
defects in the parameter range where theory predicts that steady straight rolls
should be stable. The correlation length of the pattern decreased rapidly with
increasing control parameter so that the size of a correlated area became much
smaller than the area of the cell. This suggests that the chaotic behavior is
intrinsic to large aspect ratio geometries.Comment: Preprint of experimental paper submitted to Phys. Rev. Lett. May 12
1993. Text is preceeded by many TeX macros. Figures 1 and 2 are rather lon
Numerical and Experimental Investigation of Circulation in Short Cylinders
In preparation for an experimental study of magnetorotational instability
(MRI) in liquid metal, we explore Couette flows having height comparable to the
gap between cylinders, centrifugally stable rotation, and high Reynolds number.
Experiments in water are compared with numerical simulations. Simulations show
that endcaps corotating with the outer cylinder drive a strong poloidal
circulation that redistributes angular momentum. Predicted azimuthal flow
profiles agree well with experimental measurements. Spin-down times scale with
Reynolds number as expected for laminar Ekman circulation; extrapolation from
two-dimensional simulations at agrees remarkably well with
experiment at . This suggests that turbulence does not dominate
the effective viscosity. Further detailed numerical studies reveal a strong
radially inward flow near both endcaps. After turning vertically along the
inner cylinder, these flows converge at the midplane and depart the boundary in
a radial jet. To minimize this circulation in the MRI experiment, endcaps
consisting of multiple, differentially rotating rings are proposed. Simulations
predict that an adequate approximation to the ideal Couette profile can be
obtained with a few rings
Boundary Limitation of Wavenumbers in Taylor-Vortex Flow
We report experimental results for a boundary-mediated wavenumber-adjustment
mechanism and for a boundary-limited wavenumber-band of Taylor-vortex flow
(TVF). The system consists of fluid contained between two concentric cylinders
with the inner one rotating at an angular frequency . As observed
previously, the Eckhaus instability (a bulk instability) is observed and limits
the stable wavenumber band when the system is terminated axially by two rigid,
non-rotating plates. The band width is then of order at small
() and agrees well with
calculations based on the equations of motion over a wide -range.
When the cylinder axis is vertical and the upper liquid surface is free (i.e.
an air-liquid interface), vortices can be generated or expelled at the free
surface because there the phase of the structure is only weakly pinned. The
band of wavenumbers over which Taylor-vortex flow exists is then more narrow
than the stable band limited by the Eckhaus instability. At small
the boundary-mediated band-width is linear in . These results are
qualitatively consistent with theoretical predictions, but to our knowledge a
quantitative calculation for TVF with a free surface does not exist.Comment: 8 pages incl. 9 eps figures bitmap version of Fig
Shortcomings of Vitamin D-Based Model Simulations of Seasonal Influenza
Seasonal variation in serum concentration of the vitamin D metabolite 25(OH)
vitamin D [25(OH)D], which contributes to host immune function, has
been hypothesized to be the underlying source of observed influenza seasonality
in temperate regions. The objective of this study was to determine whether
observed 25(OH)D levels could be used to simulate observed influenza infection
rates. Data of mean and variance in 25(OH)D serum levels by month were obtained
from the Health Professionals Follow-up Study and used to parameterize an
individual-based model of influenza transmission dynamics in two regions of the
United States. Simulations were compared with observed daily influenza excess
mortality data. Best-fitting simulations could reproduce the observed seasonal
cycle of influenza; however, these best-fit simulations were shown to be highly
sensitive to stochastic processes within the model and were unable consistently
to reproduce observed seasonal patterns. In this respect the simulations with
the vitamin D forced model were inferior to similar modeling efforts using
absolute humidity and the school calendar as seasonal forcing variables. These
model results indicate it is unlikely that seasonal variations in vitamin D
levels principally determine the seasonality of influenza in temperate
regions
A Reversible Gene-Targeting Strategy Identifies Synthetic Lethal Interactions between MK2 and p53 in the DNA Damage Response In Vivo
A fundamental limitation in devising new therapeutic strategies for killing cancer cells with DNA damaging agents is the need to identify synthetic lethal interactions between tumor-specific mutations and components of the DNA damage response (DDR) in vivo. The stress-activated p38 mitogen-activated protein kinase (MAPK)/MAPKAP kinase-2 (MK2) pathway is a critical component of the DDR network in p53-deficient tumor cells in vitro. To explore the relevance of this pathway for cancer therapy in vivo, we developed a specific gene targeting strategy in which Cre-mediated recombination simultaneously creates isogenic MK2-proficient and MK2-deficient tumors within a single animal. This allows direct identification of MK2 synthetic lethality with mutations that promote tumor development or control response to genotoxic treatment. In an autochthonous model of non-small-cell lung cancer (NSCLC), we demonstrate that MK2 is responsible for resistance of p53-deficient tumors to cisplatin, indicating synthetic lethality between p53 and MK2 can successfully be exploited for enhanced sensitization of tumors to DNA-damaging chemotherapeutics in vivo.National Institutes of Health (U.S.) (Grant ES015339)National Institutes of Health (U.S.) (Grant GM60594)National Institutes of Health (U.S.) (Grant GM59281)National Institutes of Health (U.S.) (Grant CA112967)Janssen Pharmaceutical Ltd.Massachusetts Institute of Technology. Center for Environmental Health Sciences (Core Grant P30-CA14051)Massachusetts Institute of Technology. Center for Environmental Health Sciences (Core Grant ES-002109
The Dynamics of Disorder-Order Transition in Hard Sphere Colloidal Dispersions
The Physics of Hard Spheres Experiment (PHaSE) seeks a complete understanding of the entropically driven disorder-order transition in hard sphere colloidal dispersions. The light scattering instrument designed for flight collects Bragg and low angle light scattering in the forward direction via a CCD camera and performs conventional static and dynamic light scattering at 10-160 deg. through fiber optic cables. Here we report on the kinetics of nucleation and growth extracted from time-resolved Bragg images and measurements of the elastic modulus of crystalline phases obtained by monitoring resonant responses to sinusoidal forcing through dynamic light scattering. Preliminary analysis of the former indicates a significant difference from measurements on the ground, while the latter confirms nicely laboratory experiments with the same instrument and predictions from computer simulations
Vitamin D in the general population of young adults with autism in the Faroe Islands
Vitamin D deficiency has been proposed as a possible risk factor for developing autism spectrum disorder (ASD). 25-Hydroxyvitamin D3 (25(OH)D3) levels were examined in a cross-sectional population-based study in the Faroe Islands. The case group consisting of a total population cohort of 40 individuals with ASD (aged 15–24 years) had significantly lower 25(OH)D3 than their 62 typically-developing siblings and their 77 parents, and also significantly lower than 40 healthy age and gender matched comparisons. There was a trend for males having lower 25(OH)D3 than females. Effects of age, month/season of birth, IQ, various subcategories of ASD and Autism Diagnostic Observation Schedule score were also investigated, however, no association was found. The very low 25(OH)D3 in the ASD group suggests some underlying pathogenic mechanism
Vitamin D deficiency contributes directly to the acute respiratory distress syndrome (ARDS)
Rationale: Vitamin D deficiency has been implicated as a pathogenic factor in sepsis and intensive therapy unit mortality but has not been assessed as a risk factor for acute respiratory distress syndrome (ARDS). Causality of these associations has never been demonstrated. Objectives: To determine if ARDS is associated with vitamin D deficiency in a clinical setting and to determine if vitamin D deficiency in experimental models of ARDS influences its severity. Methods: Human, murine and in vitro primary alveolar epithelial cell work were included in this study. Findings: Vitamin D deficiency (plasma 25(OH)D levels 600 genes. In a clinical setting, pharmacological repletion of vitamin D prior to oesophagectomy reduced the observed changes of in vivo measurements of alveolar capillary damage seen in deficient patients. Conclusions: Vitamin D deficiency is common in people who develop ARDS. This deficiency of vitamin D appears to contribute to the development of the condition, and approaches to correct vitamin D deficiency in patients at risk of ARDS should be developed
Upregulation of the cell-cycle regulator RGC-32 in Epstein-Barr virus-immortalized cells
Epstein-Barr virus (EBV) is implicated in the pathogenesis of multiple human tumours of lymphoid and epithelial origin. The virus infects and immortalizes B cells establishing a persistent latent infection characterized by varying patterns of EBV latent gene expression (latency 0, I, II and III). The CDK1 activator, Response Gene to Complement-32 (RGC-32, C13ORF15), is overexpressed in colon, breast and ovarian cancer tissues and we have detected selective high-level RGC-32 protein expression in EBV-immortalized latency III cells. Significantly, we show that overexpression of RGC-32 in B cells is sufficient to disrupt G2 cell-cycle arrest consistent with activation of CDK1, implicating RGC-32 in the EBV transformation process. Surprisingly, RGC-32 mRNA is expressed at high levels in latency I Burkitt's lymphoma (BL) cells and in some EBV-negative BL cell-lines, although RGC-32 protein expression is not detectable. We show that RGC-32 mRNA expression is elevated in latency I cells due to transcriptional activation by high levels of the differentially expressed RUNX1c transcription factor. We found that proteosomal degradation or blocked cytoplasmic export of the RGC-32 message were not responsible for the lack of RGC-32 protein expression in latency I cells. Significantly, analysis of the ribosomal association of the RGC-32 mRNA in latency I and latency III cells revealed that RGC-32 transcripts were associated with multiple ribosomes in both cell-types implicating post-initiation translational repression mechanisms in the block to RGC-32 protein production in latency I cells. In summary, our results are the first to demonstrate RGC-32 protein upregulation in cells transformed by a human tumour virus and to identify post-initiation translational mechanisms as an expression control point for this key cell-cycle regulator
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