280 research outputs found

    Self-gravity as an explanation of the fractal structure of the interstellar medium

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    The gas clouds of the interstellar medium have a fractal structure, the origin of which has generally been thought to lie in turbulence. The energy of turbulence could come from galactic rotation at large-scale, then cascade down to be dissipated on small-scales by viscosity; it has been suggested that such turbulence helps to prevent massive molecular clouds from collapsing in response to their own gravity. Here we show that, on the contrary, self-gravity itself may be the dominant factor in making clouds fractal. We develop a field-theory approach to the structure of clouds, assuming them to be isothermal, and with only gravitational interactions; we find that the observed fractal dimension of the clouds arise naturally from this approach. Although this result does not imply that turbulence is not important, it does demonstrate that the fractal structure can be understood without it.Comment: Latex file, four pages and two colour figures in .cps files. To appear in Nature, 5 September 199

    Ovarian steroid hormones: what's hot in the stem cell pool?

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    The vital role of ovarian hormones in the development of the normal breast foreshadowed their importance in mammary stem cell regulation. Two recent papers reveal that 17β-estradiol and progesterone control the size and repopulating ability of the mammary stem cell compartment. This likely occurs via paracrine signaling from steroid receptor-positive luminal cells to steroid receptor-negative stem cells. These findings illuminate roles for the female sex steroids in mobilizing the stem cell pool in the normal breast, and also provide a crucial link between the known hormonal risks of breast cancer and the potential stem cell origin of this disease

    Small but crucial : the novel small heat shock protein Hsp21 mediates stress adaptation and virulence in Candida albicans

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    Peer reviewedPublisher PD

    Long-Term Functional Side-Effects of Stimulants and Sedatives in Drosophila melanogaster

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    Background: Small invertebrate animals, such as nematodes and fruit flies, are increasingly being used to test candidate drugs both for specific therapeutic purposes and for long-term health effects. Some of the protocols used in these experiments feature such experimental design features as lifelong virginity and very low densities. By contrast, the ability of both fruit flies and nematodes to resist stress is frequently correlated with their longevity and other functional measures, suggesting that low-stress assays are not necessarily the only useful protocol for testing the long-term effects of drugs. Methodology/Principal Findings: Here we report an alternative protocol for fruit fly drug-testing that maximizes reproductive opportunities and other types of interaction, with moderately high population densities. We validate this protocol using two types of experimental tests: 1. We show that this protocol detects previously well-established genetic differences between outbred fruit fly populations. 2. We show that this protocol is able to distinguish among the long-term effects of similar types of drugs within two broad categories, stimulants and tranquilizers. Conclusions: Large-scale fly drug testing can be conducted using mixed-sex high-density cage assays. We find that the commonly-used stimulants caffeine and theobromine differ dramatically in their chronic functional effects, theobromine being more benign. Likewise, we find that two generic pharmaceutical tranquilizers, lithium carbonate and valproic acid, differ dramatically in their chronic effects, lithium being more benign. However, these findings do not necessarily apply t

    Src tyrosine kinase augments taxotere-induced apoptosis through enhanced expression and phosphorylation of Bcl-2

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    Activation of Src, which has an intrinsic protein tyrosine kinase activity, has been demonstrated in many human tumours, such as colorectal and breast cancers, and is closely associated with the pathogenesis and metastatic potential of these cancers. In this study, we have examined the effect of activated Src on the sensitivity to taxotere, an anticancer drug targeting microtubules, using v-src-transfected HAG-1 human gall bladder epithelial cells. As compared with parental HAG-1 cell line, v-src-transfected HAG/src3-1 cells became 5.9 and 7.0-fold sensitive to taxotere for 2 and 24-h exposure, respectively. By contrast, HAG-1 cells transfected with activated Ras, which acts downstream of Src, acquired approximately 2.5∼4.8-fold taxotere resistance. The taxotere sensitivity in HAG/src3-1 cells was reversed, if not completely, by herbimycin A, a specific inhibitor of Src family protein tyrosine kinase, indicating that Src protein tyrosine kinase augments sensitivity to taxotere. Treatment of HAG/src3-1 cells with taxotere resulted in phosphorylation of Bcl-2 and subsequent induction of apoptotic cell death, whereas neither Bcl-2 phosphorylation nor apoptosis occurred in parental or c-H-ras-transfected HAG-1 cells. Interestingly, the Bcl-2 protein is overexpressed in v-src-transfected cell line, compared to those in parental or Ras-transfected cell line. Treatment of HAG/src3-1 cells with herbimycin A significantly reduced the expression and phosphorylation of Bcl-2, and abrogated taxotere-induced apoptosis, suggesting a potential role for Src protein tyrosine kinase in the taxotere-induced apoptotic events. H-7, a protein kinase C inhibitor and wortmannin, a phosphatidylinositol-3 kinase (PI-3 kinase) inhibitor, neither altered taxotere sensitivity nor inhibited taxotere-induced apoptosis in these cells. These data indicate that the ability of activated Src to increase taxotere sensitivity would be mediated by apoptotic events occurring through Src to downstream signal transduction pathways toward Bcl-2 phosphorylation, but not by activated Ras, PI-3 kinase or protein kinase C

    Fractal Dimensions and Scaling Laws in the Interstellar Medium and Galaxy Distributions: a new Field Theory Approach

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    We develop a field theoretical approach to the cold interstellar medium (ISM) and large structure of the universe. We show that a non-relativistic self- gravitating gas in thermal equilibrium with variable number of atoms or fragments is exactly equivalent to a field theory of a scalar field phi(x) with exponential self-interaction. We analyze this field theory perturbatively and non-perturbatively through the renormalization group(RG).We show scaling behaviour (critical) for a continuous range of the physical parameters as the temperature. We derive in this framework the scaling relation M(R) \sim R^{d_H} for the mass on a region of size R, and Delta v \sim R^\frac12(d_H -1) for the velocity dispersion. For the density-density correlations we find a power-law behaviour for large distances \sim |r_1 - r_2|^{2D - 6}.The fractal dimension D turns to be related with the critical exponent \nu by D = 1/ \nu. Mean field theory yields \nu = 1/2, D = 2. Both the Ising and the mean field values are compatible with the present ISM observational data:1.4\leq D \leq 2. We develop a field theoretical approach to the galaxy distribution considering a gas of self-gravitating masses on the FRW background, in quasi-thermal equi- librium. We show that it exhibits scaling behaviour by RG methods. The galaxy correlations are computed without assuming homogeneity. We find \sim r^{D-3} .Thetheoryallowstocomputethethreeandhigherdensitycorrelatorswithoutanyassumption.WefindthattheconnectedNpointsdensityscalesasr1N(D3),when. The theory allows to compute the three and higher density correlators without any assumption.We find that the connected N-points density scales as r_1^{N(D-3)}, when r_1 >> r_i

    Comparative quantification of health risks: Conceptual framework and methodological issues

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    Reliable and comparable analysis of risks to health is key for preventing disease and injury. Causal attribution of morbidity and mortality to risk factors has traditionally been conducted in the context of methodological traditions of individual risk factors, often in a limited number of settings, restricting comparability. In this paper, we discuss the conceptual and methodological issues for quantifying the population health effects of individual or groups of risk factors in various levels of causality using knowledge from different scientific disciplines. The issues include: comparing the burden of disease due to the observed exposure distribution in a population with the burden from a hypothetical distribution or series of distributions, rather than a single reference level such as non-exposed; considering the multiple stages in the causal network of interactions among risk factor(s) and disease outcome to allow making inferences about some combinations of risk factors for which epidemiological studies have not been conducted, including the joint effects of multiple risk factors; calculating the health loss due to risk factor(s) as a time-indexed "stream" of disease burden due to a time-indexed "stream" of exposure, including consideration of discounting; and the sources of uncertainty
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