71 research outputs found

    Resolved Kennicutt-Schmidt Law in Nearby Galaxies

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    The Kennicutt-Schmidt law (Schmidt 1959; Kennicutt 1998, hereafter K-S law) is a power law correlation between area averaged star formation rate (Σ_(SFR)) and gas surface density (Σ_(gas)). Despite its importance, the physics that underlie this correlation has remained unclear. The power law index, N, is a prime discriminator of the mechanisms that regulate star formation and form the K-S law (e.g. Leroy et al. 2008; Tan 2010). We present a study of the resolved K-S law for 10 nearby disk galaxies using our new CO(1-0) data at 750 and 500 pc resolutions. The CO(1-0) line emission is established as a tracer of the molecular gas column density, and results in a super-linear correlation (N = 1.3 and 1.8). We discuss the cause of the discrepancy between previous studies, and the mechanism of star formation indicated from our new results

    Resolved Kennicutt-Schmidt Law in Nearby Galaxies

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    The Kennicutt-Schmidt law (Schmidt 1959; Kennicutt 1998, hereafter K-S law) is a power law correlation between area averaged star formation rate (Σ_(SFR)) and gas surface density (Σ_(gas)). Despite its importance, the physics that underlie this correlation has remained unclear. The power law index, N, is a prime discriminator of the mechanisms that regulate star formation and form the K-S law (e.g. Leroy et al. 2008; Tan 2010). We present a study of the resolved K-S law for 10 nearby disk galaxies using our new CO(1-0) data at 750 and 500 pc resolutions. The CO(1-0) line emission is established as a tracer of the molecular gas column density, and results in a super-linear correlation (N = 1.3 and 1.8). We discuss the cause of the discrepancy between previous studies, and the mechanism of star formation indicated from our new results

    Inter- and intraobserver reliability of the MTM-classification for proximal humeral fractures: A prospective study

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    <p>Abstract</p> <p>Background</p> <p>A precise modular topographic-morphological (MTM) classification for proximal humeral fractures may address current classification problems. The classification was developed to evaluate whether a very detailed classification exceeding the analysis of fractured parts may be a valuable tool.</p> <p>Methods</p> <p>Three observers classified plain radiographs of 22 fractures using both a simple version (fracture displacement, number of parts) and an extensive version (individual topographic fracture type and morphology) of the MTM classification. Kappa-statistics were used to determine reliability.</p> <p>Results</p> <p>An acceptable reliability was found for the simple version classifying fracture displacement and fractured main parts. Fair interobserver agreement was found for the extensive version with individual topographic fracture type and morphology.</p> <p>Conclusion</p> <p>Although the MTM-classification covers a wide spectrum of fracture types, our results indicate that the precise topographic and morphological description is not delivering reproducible results. Therefore, simplicity in fracture classification may be more useful than extensive approaches, which are not adequately reliable to address current classification problems.</p

    Single-channel properties of a stretch-sensitive chloride channel in the human mast cell line HMC-1

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    A stretch-activated (SA) Cl− channel in the plasma membrane of the human mast cell line HMC-1 was identified in outside-out patch-clamp experiments. SA currents, induced by pressure applied to the pipette, exhibited voltage dependence with strong outward rectification (55.1 pS at +100 mV and an about tenfold lower conductance at −100 mV). The probability of the SA channel being open (Po) also showed steep outward rectification and pressure dependence. The open-time distribution was fitted with three components with time constants of τ1o = 755.1 ms, τ2o = 166.4 ms, and τ3o = 16.5 ms at +60 mV. The closed-time distribution also required three components with time constants of τ1c = 661.6 ms, τ2c = 253.2 ms, and τ3c = 5.6 ms at +60 mV. Lowering extracellular Cl− concentration reduced the conductance, shifted the reversal potential toward chloride reversal potential, and decreased the Po at positive potentials. The SA Cl− currents were reversibly blocked by the chloride channel blocker 4,4′-diisothiocyanatostilbene-2,2′-disulfonic acid (DIDS) but not by (Z)-1-(p-dimethylaminoethoxyphenyl)-1,2-diphenyl-1-butene (tamoxifen). Furthermore, in HMC-1 cells swelling due to osmotic stress, DIDS could inhibit the increase in intracellular [Ca2+] and degranulation. We conclude that in the HMC-1 cell line, the SA outward currents are mediated by Cl− influx. The SA Cl− channel might contribute to mast cell degranulation caused by mechanical stimuli or accelerate membrane fusion during the degranulation process

    Molecular Gas and Star Formation in Nearby Disk Galaxies

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    We compare molecular gas traced by ^(12)CO (2-1) maps from the HERACLES survey, with tracers of the recent star formation rate (SFR) across 30 nearby disk galaxies. We demonstrate a first-order linear correspondence between Σ_(mol) and Σ_(SFR) but also find important second-order systematic variations in the apparent molecular gas depletion time, τ_(dep)^(mol) = ∑_(mol)/∑_(SFR). At the 1 kpc common resolution of HERACLES, CO emission correlates closely with many tracers of the recent SFR. Weighting each line of sight equally, using a fixed α_(CO) equivalent to the Milky Way value, our data yield a molecular gas depletion time, τ_(dep)^(mol)= ∑_(mol)∑_(SFR) ≈ 2.2 Gyr with 0.3 dex 1σ scatter, in very good agreement with recent literature data. We apply a forward-modeling approach to constrain the power-law index, N, that relates the SFR surface density and the molecular gas surface density, ∑_(SFR) ∝ ∑_(mol)^N. We find N = 1 ± 0.15 for our full data set with some scatter from galaxy to galaxy. This also agrees with recent work, but we caution that a power-law treatment oversimplifies the topic given that we observe correlations between τ_(dep)^(mol) and other local and global quantities. The strongest of these are a decreased τ_(dep)^(mol) in low-mass, low-metallicity galaxies and a correlation of the kpc-scale τ_(dep)^(mol) with dust-to-gas ratio, D/G. These correlations can be explained by a CO-to-H_2 conversion factor (α_(CO)) that depends on dust shielding, and thus D/G, in the theoretically expected way. This is not a unique interpretation, but external evidence of conversion factor variations makes this the most conservative explanation of the strongest observed τ_(dep)^(mol) trends. After applying a D/G-dependent α_(CO), some weak correlations between τ_(dep)^(mol) and local conditions persist. In particular, we observe lower τ_(dep)^(mol) and enhanced CO excitation associated with nuclear gas concentrations in a subset of our targets. These appear to reflect real enhancements in the rate of star formation per unit gas, and although the distribution of τ_(dep) does not appear bimodal in galaxy centers, τ_(dep) does appear multivalued at fixed Σ_(H2), supporting the idea of "disk" and "starburst" modes driven by other environmental parameters

    Search for leptophobic Z ' bosons decaying into four-lepton final states in proton-proton collisions at root s=8 TeV

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    Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

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    In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. For example, a key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process versus those that measure fl ux through the autophagy pathway (i.e., the complete process including the amount and rate of cargo sequestered and degraded). In particular, a block in macroautophagy that results in autophagosome accumulation must be differentiated from stimuli that increase autophagic activity, defi ned as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (inmost higher eukaryotes and some protists such as Dictyostelium ) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the fi eld understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. It is worth emphasizing here that lysosomal digestion is a stage of autophagy and evaluating its competence is a crucial part of the evaluation of autophagic flux, or complete autophagy. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. Along these lines, because of the potential for pleiotropic effects due to blocking autophagy through genetic manipulation it is imperative to delete or knock down more than one autophagy-related gene. In addition, some individual Atg proteins, or groups of proteins, are involved in other cellular pathways so not all Atg proteins can be used as a specific marker for an autophagic process. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field
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