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

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

Extended [C I] and (CO)-C-13 (5 -\u3e 4) emission in M17SW

We mapped a 13 × 22 pc region in emission from 492 GHz [C I] and, for the first time, 551 GHz 13CO (5 → 4) in the giant molecular cloud M17SW. The morphologies of the [C I] and 13CO emission are strikingly similar. The extent and intensity of the [C I] and 13CO (5 → 4) emission is explained as arising from photodissociation regions on the surfaces of embedded molecular clumps. Modeling of the 13CO (5 → 4) emission in comparison to 13CO (1 → 0) indicates a temperature gradient across the cloud, peaking to at least 63 K near the M17 ionization front and decreasing to at least 20 K at the western edge of the cloud. We see no correlation between gas density and column density. The beam-averaged column density of C I in the core is 1 × 1018 cm-2, and the mean column density ratio N(C I)/N(CO) is about 0.4. The variations of N(C I)/N(CO) with position in M17SW indicate a similar clump size distribution throughout the cloud

Inhibition of TGF-β Signaling and Decreased Apoptosis in IUGR-Associated Lung Disease in Rats

Intrauterine growth restriction is associated with impaired lung function in adulthood. It is unknown whether such impairment of lung function is linked to the transforming growth factor (TGF)-β system in the lung. Therefore, we investigated the effects of IUGR on lung function, expression of extracellular matrix (ECM) components and TGF-β signaling in rats. IUGR was induced in rats by isocaloric protein restriction during gestation. Lung function was assessed with direct plethysmography at postnatal day (P) 70. Pulmonary activity of the TGF-β system was determined at P1 and P70. TGF-β signaling was blocked in vitro using adenovirus-delivered Smad7. At P70, respiratory airway compliance was significantly impaired after IUGR. These changes were accompanied by decreased expression of TGF-β1 at P1 and P70 and a consistently dampened phosphorylation of Smad2 and Smad3. Furthermore, the mRNA expression levels of inhibitors of TGF-β signaling (Smad7 and Smurf2) were reduced, and the expression of TGF-β-regulated ECM components (e.g. collagen I) was decreased in the lungs of IUGR animals at P1; whereas elastin and tenascin N expression was significantly upregulated. In vitro inhibition of TGF-β signaling in NIH/3T3, MLE 12 and endothelial cells by adenovirus-delivered Smad7 demonstrated a direct effect on the expression of ECM components. Taken together, these data demonstrate a significant impact of IUGR on lung development and function and suggest that attenuated TGF-β signaling may contribute to the pathological processes of IUGR-associated lung disease

First- and second-order contributions to depth perception in anti-correlated random dot stereograms.

The binocular energy model of neural responses predicts that depth from binocular disparity might be perceived in the reversed direction when the contrast of dots presented to one eye is reversed. While reversed-depth has been found using anti-correlated random-dot stereograms (ACRDS) the findings are inconsistent across studies. The mixed findings may be accounted for by the presence of a gap between the target and surround, or as a result of overlap of dots around the vertical edges of the stimuli. To test this, we assessed whether (1) the gap size (0, 19.2 or 38.4 arc min) (2) the correlation of dots or (3) the border orientation (circular target, or horizontal or vertical edge) affected the perception of depth. Reversed-depth from ACRDS (circular no-gap condition) was seen by a minority of participants, but this effect reduced as the gap size increased. Depth was mostly perceived in the correct direction for ACRDS edge stimuli, with the effect increasing with the gap size. The inconsistency across conditions can be accounted for by the relative reliability of first- and second-order depth detection mechanisms, and the coarse spatial resolution of the latter

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

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} $. The theory allows to compute the three and higher density correlators without any assumption.We find that the connected N-points density scales as r_1^{N(D-3)}, when$ r_1 >> r_i

MicroRNA Involvement in Immune Activation During Heart Failure

Heart failure is one of the common end stages of cardiovascular diseases, the leading cause of death in developed countries. Molecular mechanisms underlying the development of heart failure remain elusive but there is a consistent observation of chronic immune activation and aberrant microRNA (miRNA) expression that is present in failing hearts. This review will focus on the interplay between the immune system and miRNAs as factors that play a role during the development of heart failure. Several studies have shown that heart failure patients can be characterized by a sustained innate immune activation. The role of inflammatory signaling is discussed and TLR4 signaling, IL-1β, TNFα and IL-6 expression appears to coincide with the development of heart failure. Furthermore, we describe the implication of the renin angiotensin aldosteron system in immunity and heart failure. In the past decade microRNAs (miRNAs), small non-coding RNAs that translationally repress protein synthesis by binding to partially complementary sequences of mRNA, have come to light as important regulators of several kinds of cardiovascular diseases including cardiac hypertrophy and heart failure. The involvement of differentially expressed miRNAs in the inflammation that occurs during the development of heart failure is still subject of investigation. Here, we summarize and comment on the first studies in this field and hypothesize on the putative involvement of certain miRNAs in heart failure. MicroRNAs have been shown to be critical regulators of cardiac function and inflammation. Future research will have to point out if dampening the immune response, and the miRNAs associated with it, during the development of heart failure is a therapeutically plausible route to follow

Lack of Chemokine Signaling through CXCR5 Causes Increased Mortality, Ventricular Dilatation and Deranged Matrix during Cardiac Pressure Overload

RATIONALE: Inflammatory mechanisms have been suggested to play a role in the development of heart failure (HF), but a role for chemokines is largely unknown. Based on their role in inflammation and matrix remodeling in other tissues, we hypothesized that CXCL13 and CXCR5 could be involved in cardiac remodeling during HF. OBJECTIVE: We sought to analyze the role of the chemokine CXCL13 and its receptor CXCR5 in cardiac pathophysiology leading to HF. METHODS AND RESULTS: Mice harboring a systemic knockout of the CXCR5 (CXCR5(-/-)) displayed increased mortality during a follow-up of 80 days after aortic banding (AB). Following three weeks of AB, CXCR5(-/-) developed significant left ventricular (LV) dilatation compared to wild type (WT) mice. Microarray analysis revealed altered expression of several small leucine-rich proteoglycans (SLRPs) that bind to collagen and modulate fibril assembly. Protein levels of fibromodulin, decorin and lumican (all SLRPs) were significantly reduced in AB CXCR5(-/-) compared to AB WT mice. Electron microscopy revealed loosely packed extracellular matrix with individual collagen fibers and small networks of proteoglycans in AB CXCR5(-/-) mice. Addition of CXCL13 to cultured cardiac fibroblasts enhanced the expression of SLRPs. In patients with HF, we observed increased myocardial levels of CXCR5 and SLRPs, which was reversed following LV assist device treatment. CONCLUSIONS: Lack of CXCR5 leads to LV dilatation and increased mortality during pressure overload, possibly via lack of an increase in SLRPs. This study demonstrates a critical role of the chemokine CXCL13 and CXCR5 in survival and maintaining of cardiac structure upon pressure overload, by regulating proteoglycans essential for correct collagen assembly

Pediatric T- and NK-cell lymphomas: new biologic insights and treatment strategies

T- and natural killer (NK)-cell lymphomas are challenging childhood neoplasms. These cancers have varying presentations, vast molecular heterogeneity, and several are quite unusual in the West, creating diagnostic challenges. Over 20 distinct T- and NK-cell neoplasms are recognized by the 2008 World Health Organization classification, demonstrating the diversity and potential complexity of these cases. In pediatric populations, selection of optimal therapy poses an additional quandary, as most of these malignancies have not been studied in large randomized clinical trials. Despite their rarity, exciting molecular discoveries are yielding insights into these clinicopathologic entities, improving the accuracy of our diagnoses of these cancers, and expanding our ability to effectively treat them, including the use of new targeted therapies. Here, we summarize this fascinating group of lymphomas, with particular attention to the three most common subtypes: T-lymphoblastic lymphoma, anaplastic large cell lymphoma, and peripheral T-cell lymphoma-not otherwise specified. We highlight recent findings regarding their molecular etiologies, new biologic markers, and cutting-edge therapeutic strategies applied to this intriguing class of neoplasms