Starting of rocket engine at conditions of simulated altitude using crude monoethylaniline and other fuels with mixed acid

Experiments were conducted at sea level and pressure altitude of about 55,000 feet at various temperatures to determine starting characteristics of a commercial rocket engine using crude monoethylaniline and other fuels with mixed acid. With crude monoethylaniline, ignition difficulties were encountered at temperatures below about 20 degrees F. With mixed butyl mercaptans, water-white turpentine, and x-pinene, no starting difficulties were experienced at temperatures as low as minus 74 degrees F. Turpentine and x-pinene, however, sometimes left deposits on the injector face. With blends containing furfuryl alcohol and with other blends, difficulties were experienced either from appreciable deposits or from starting

Cross-over behaviour in a communication network

We address the problem of message transfer in a communication network. The network consists of nodes and links, with the nodes lying on a two dimensional lattice. Each node has connections with its nearest neighbours, whereas some special nodes, which are designated as hubs, have connections to all the sites within a certain area of influence. The degree distribution for this network is bimodal in nature and has finite variance. The distribution of travel times between two sites situated at a fixed distance on this lattice shows fat fractal behaviour as a function of hub-density. If extra assortative connections are now introduced between the hubs so that each hub is connected to two or three other hubs, the distribution crosses over to power-law behaviour. Cross-over behaviour is also seen if end-to-end short cuts are introduced between hubs whose areas of influence overlap, but this is much milder in nature. In yet another information transmission process, namely, the spread of infection on the network with assortative connections, we again observed cross-over behaviour of another type, viz. from one power-law to another for the threshold values of disease transmission probability. Our results are relevant for the understanding of the role of network topology in information spread processes.Comment: 12 figure

Nodular fasciitis: a comprehensive, time-correlated investigation of 17 cases

The self-limited nature of nodular fasciitis (NF) is well-known but its precise mechanism has not yet been clarified. We observed that "young" NF (preoperative duration 3 months) (similar to 20%). Thus, we hypothesized that our original observation may reflect a connection with the self-limited nature of NF. Seventeen cases with reliable data concerning the onset were selected, thus approximating the lifetime of each tumor. Besides the USP6 interphase FISH examination, we also checked the most common MYH9-USP6 fusion using RT-PCR. Because of the known pathways of the tumorigenesis of NF, the mRNA level of USP6, TRAIL, IFN-beta, JAK1, STAT1, STAT3, JUN, and CDKN2A was measured using qRT-PCR. Regarding proteins, USP6, p16, p27, TRAIL, and IFN-beta were examined using immunohistochemistry. Targeted gene panel next-generation sequencing (NGS) of three cases was additionally performed. We found a strong negative correlation (p = 0.000) between the lifetime and percentage of USP6 break-apart signals and a strong positive relationship (p = 0.000) between USP6 break-apart signals and mitotic counts. Results of immunostainings, along with qRT-PCR results, favored the previously-suggested USP6-induced negative feedback mechanism through activation of TRAIL and IFN-beta, likely resulting in apoptosis and senescence of tumor cells harboring USP6 fusions. Targeted-NGS resulted in the detection of several variants, but no additional recurrent changes in the pathogenesis of these tumors. We revealed on a cellular level the USP6-induced negative feedback mechanism. In conclusion, we emphasize that in "old" NF, the percentage of USP6 break-apart FISH signals can be as low as 14-27% which can be very important from a differential diagnostic point of view. We emphasize that a careful examination and interpretation of the NGS data is needed before clinical decision-making on treatment.Cancer Signaling networks and Molecular Therapeutic

Wildlife Trade and Global Disease Emergence

The global trade in wildlife provides disease transmission mechanisms that not only cause human disease outbreaks but also threaten livestock, international trade, rural livelihoods, native wildlife populations, and the health of ecosystems. Outbreaks resulting from wildlife trade have caused hundreds of billions of dollars of economic damage globally. Rather than attempting to eradicate pathogens or the wild species that may harbor them, a practical approach would include decreasing the contact rate among species, including humans, at the interface created by the wildlife trade. Since wildlife marketing functions as a system of scale-free networks with major hubs, these points provide control opportunities to maximize the effects of regulatory efforts

PRMT1 and PRMT8 regulate retinoic acid-dependent neuronal differentiation with implications to neuropathology.

Retinoids are morphogens and have been implicated in cell fate commitment of embryonic stem cells (ESCs) to neurons. Their effects are mediated by RAR and RXR nuclear receptors. However, transcriptional cofactors required for cell and gene-specific retinoid signaling are not known. Here we show that protein arginine methyl transferase (PRMT) 1 and 8 have key roles in determining retinoid regulated gene expression and cellular specification in a multistage neuronal differentiation model of murine ESCs. PRMT1 acts as a selective modulator, providing the cells with a mechanism to reduce the potency of retinoid signals on regulatory "hotspots." PRMT8 is a retinoid receptor target gene itself and acts as a cell type specific transcriptional coactivator of retinoid signaling at later stages of differentiation. Lack of either of them leads to reduced nuclear arginine methylation, dysregulated neuronal gene expression, and altered neuronal activity. Importantly, depletion of PRMT8 results in altered expression of a distinct set of genes, including markers of gliomagenesis. PRMT8 is almost entirely absent in human glioblastoma tissues. We propose that PRMT1 and PRMT8 serve as a rheostat of retinoid signaling to determine neuronal cell specification in a context-dependent manner and might also be relevant in the development of human brain malignancy

System size and centrality dependence of the balance function in A+A collisions at sqrt[sNN]=17.2 GeV

Electric charge correlations were studied for p+p, C+C, Si+Si, and centrality selected Pb+Pb collisions at sqrt[sNN]=17.2 GeV with the NA49 large acceptance detector at the CERN SPS. In particular, long-range pseudorapidity correlations of oppositely charged particles were measured using the balance function method. The width of the balance function decreases with increasing system size and centrality of the reactions. This decrease could be related to an increasing delay of hadronization in central Pb+Pb collisions

Generation-by-Generation Dissection of the Response Function in Long Memory Epidemic Processes

In a number of natural and social systems, the response to an exogenous shock relaxes back to the average level according to a long-memory kernel $\sim 1/t^{1+\theta}$ with $0 \leq \theta <1$. In the presence of an epidemic-like process of triggered shocks developing in a cascade of generations at or close to criticality, this "bare" kernel is renormalized into an even slower decaying response function $\sim 1/t^{1-\theta}$. Surprisingly, this means that the shorter the memory of the bare kernel (the larger $1+\theta$), the longer the memory of the response function (the smaller $1-\theta$). Here, we present a detailed investigation of this paradoxical behavior based on a generation-by-generation decomposition of the total response function, the use of Laplace transforms and of "anomalous" scaling arguments. The paradox is explained by the fact that the number of triggered generations grows anomalously with time at $\sim t^\theta$ so that the contributions of active generations up to time $t$ more than compensate the shorter memory associated with a larger exponent $\theta$. This anomalous scaling results fundamentally from the property that the expected waiting time is infinite for $0 \leq \theta \leq 1$. The techniques developed here are also applied to the case $\theta >1$ and we find in this case that the total renormalized response is a {\bf constant} for $t < 1/(1-n)$ followed by a cross-over to $\sim 1/t^{1+\theta}$ for $t \gg 1/(1-n)$.Comment: 27 pages, 4 figure