Wind reversals in turbulent Rayleigh-Benard convection

The phenomenon of irregular cessation and subsequent reversal of the large-scale circulation in turbulent Rayleigh-B\'enard convection is theoretically analysed. The force and thermal balance on a single plume detached from the thermal boundary layer yields a set of coupled nonlinear equations, whose dynamics is related to the Lorenz equations. For Prandtl and Rayleigh numbers in the range $10^{-2} \leq \Pr \leq 10^{3}$ and 10^{7} \leq \Ra \leq 10^{12}, the model has the following features: (i) chaotic reversals may be exhibited at Ra $\geq 10^{7}$; (ii) the Reynolds number based on the root mean square velocity scales as \Re_{rms} \sim \Ra^{[0.41 ... 0.47]} (depending on Pr), and as $\Re_{rms} \sim \Pr^{-[0.66 ... 0.76]}$ (depending on Ra); and (iii) the mean reversal frequency follows an effective scaling law \omega / (\nu L^{-2}) \sim \Pr^{-(0.64 \pm 0.01)} \Ra^{0.44 \pm 0.01}. The phase diagram of the model is sketched, and the observed transitions are discussed.Comment: 4 pages, 5 figure

Hysteresis phenomenon in turbulent convection

Coherent large-scale circulations of turbulent thermal convection in air have been studied experimentally in a rectangular box heated from below and cooled from above using Particle Image Velocimetry. The hysteresis phenomenon in turbulent convection was found by varying the temperature difference between the bottom and the top walls of the chamber (the Rayleigh number was changed within the range of $10^7 - 10^8$). The hysteresis loop comprises the one-cell and two-cells flow patterns while the aspect ratio is kept constant ($A=2 - 2.23$). We found that the change of the sign of the degree of the anisotropy of turbulence was accompanied by the change of the flow pattern. The developed theory of coherent structures in turbulent convection (Elperin et al. 2002; 2005) is in agreement with the experimental observations. The observed coherent structures are superimposed on a small-scale turbulent convection. The redistribution of the turbulent heat flux plays a crucial role in the formation of coherent large-scale circulations in turbulent convection.Comment: 10 pages, 9 figures, REVTEX4, Experiments in Fluids, 2006, in pres

Seasonal prediction skill of winter temperature over North India

This document is the Accepted Manuscript version of the following article: Tiwari, P.R., Kar, S.C., Mohanty, U.C. et al. Theor Appl Climatol (2016) 124: 15. The final publication is available at Springer via https://doi.org/10.1007/s00704-015-1397-y. © Springer-Verlag Wien 2015.The climatology, amplitude error, phase error, and mean square skill score (MSSS) of temperature predictions from five different state-of-the-art general circulation models (GCMs) have been examined for the winter (December–January– February) seasons over North India. In this region, temperature variability affects the phenological development processes of wheat crops and the grain yield. The GCM forecasts of temperature for a whole season issued in November from various organizations are compared with observed gridded temperature data obtained from the India Meteorological Department (IMD) for the period 1982–2009. The MSSS indicates that the models have skills of varying degrees. Predictions of maximum and minimum temperature obtained from the National Centers for Environmental Prediction (NCEP) climate forecast system model (NCEP_CFSv2) are compared with station level observations from the Snow and Avalanche Study Establishment (SASE). It has been found that when the model temperatures are corrected to account the bias in the model and actual orography, the predictions are able to delineate the observed trend compared to the trend without orography correction.Peer reviewedFinal Accepted Versio

Clinical array-based karyotyping of breast cancer with equivocal HER2 status resolves gene copy number and reveals chromosome 17 complexity

<p>Abstract</p> <p>Background</p> <p><it>HER2 </it>gene copy status, and concomitant administration of trastuzumab (Herceptin), remains one of the best examples of targeted cancer therapy based on understanding the genomic etiology of disease. However, newly diagnosed breast cancer cases with equivocal HER2 results present a challenge for the oncologist who must make treatment decisions despite the patient's unresolved HER2 status. In some cases both immunohistochemistry (IHC) and fluorescence <it>in situ </it>hybridization (FISH) are reported as equivocal, whereas in other cases IHC results and FISH are discordant for positive versus negative results. The recent validation of array-based, molecular karyotyping for clinical oncology testing provides an alternative method for determination of HER2 gene copy number status in cases remaining unresolved by traditional methods.</p> <p>Methods</p> <p>In the current study, DNA extracted from 20 formalin fixed paraffin embedded (FFPE) tissue samples from newly diagnosed cases of invasive ductal carcinoma referred to our laboratory with unresolved HER2 status, were analyzed using a clinically validated genomic array containing 127 probes covering the HER2 amplicon, the pericentromeric regions, and both chromosome 17 arms.</p> <p>Results</p> <p>Array-based comparative genomic hybridization (array CGH) analysis of chromosome 17 resolved HER2 gene status in [20/20] (100%) of cases and revealed additional chromosome 17 copy number changes in [18/20] (90%) of cases. Array CGH analysis also revealed two false positives and one false negative by FISH due to "ratio skewing" caused by chromosomal gains and losses in the centromeric region. All cases with complex rearrangements of chromosome 17 showed genome-wide chromosomal instability.</p> <p>Conclusions</p> <p>These results illustrate the analytical power of array-based genomic analysis as a clinical laboratory technique for resolution of HER2 status in breast cancer cases with equivocal results. The frequency of complex chromosome 17 abnormalities in these cases suggests that the two probe FISH interphase analysis is inadequate and results interpreted using the HER2/CEP17 ratio should be reported "with caution" when the presence of centromeric amplification or monosomy is suspected by FISH signal gains or losses. The presence of these pericentromeric copy number changes may result in artificial skewing of the HER2/CEP17 ratio towards false negative or false positive results in breast cancer with chromosome 17 complexity. Full genomic analysis should be considered in all cases with complex chromosome 17 aneusomy as these cases are likely to have genome-wide instability, amplifications, and a poor prognosis.</p

Relationship between the expansion of drylands and the intensification of Hadley circulation during the late twentieth century

The changes in coverage by arid climate and intensity of the Hadley circulation during the second half of the twentieth century were examined using observations and the multi-model ensemble (MME) mean of Twentieth-Century Coupled Climate Model (20C3M) simulations. It was found that the area of dry climate, which comprises steppe and desert climates following the K&#246;ppen climate classification, expanded to an appreciable extent in observation and, to a lesser degree, in MME simulation. The areal extent of steppe climate (the outer boundary of arid climate) tends to encroach on the surrounding climate groups, which, in turn, feeds desert climate (the inner part of arid climate) and causes it to grow. This result indicates the importance of accurate prediction for climate regimes that border steppe climate. Concomitant with the expansion of drylands, the observed intensity of the Hadley cell is persistently enhanced, particularly during boreal winter, suggesting the validity of a self-induction of deserts through a positive biogeophysical feedback (also known as Charney’s cycle). In comparison, the simulated Hadley circulation in the MME mean remains invariant in time. The current climate models, therefore, disagree with the observation in the long-term linkage between desertification and Hadley cell. Finally, the implication of such discrepancy is discussed as a possible guidance to improve models

Human malarial disease: a consequence of inflammatory cytokine release

Malaria causes an acute systemic human disease that bears many similarities, both clinically and mechanistically, to those caused by bacteria, rickettsia, and viruses. Over the past few decades, a literature has emerged that argues for most of the pathology seen in all of these infectious diseases being explained by activation of the inflammatory system, with the balance between the pro and anti-inflammatory cytokines being tipped towards the onset of systemic inflammation. Although not often expressed in energy terms, there is, when reduced to biochemical essentials, wide agreement that infection with falciparum malaria is often fatal because mitochondria are unable to generate enough ATP to maintain normal cellular function. Most, however, would contend that this largely occurs because sequestered parasitized red cells prevent sufficient oxygen getting to where it is needed. This review considers the evidence that an equally or more important way ATP deficency arises in malaria, as well as these other infectious diseases, is an inability of mitochondria, through the effects of inflammatory cytokines on their function, to utilise available oxygen. This activity of these cytokines, plus their capacity to control the pathways through which oxygen supply to mitochondria are restricted (particularly through directing sequestration and driving anaemia), combine to make falciparum malaria primarily an inflammatory cytokine-driven disease