Near-infrared reddening of extra-galactic GMCs in a face-on geometry

[Abridged] We describe the near-infrared reddening signature of giant molecular clouds (GMCs) in external galaxies. In particular, we examine the E(J-H) and E(H-K) color-excesses, and the effective extinction law observed in discrete GMC regions. We also study the effect of the relative scale height of the GMC distribution to the color-excesses, and to the observed mass function of GMCs. We perform Monte Carlo radiative transfer simulations with 3D models of stellar radiation and clumpy dust distributions, resembling a face-on geometry. The scattered light is included in the models, and near-infrared color maps are calculated from the simulated data. The effective near-infrared reddening law, i.e. the ratio E(J-H)/E(H-K), has a value close to unity in GMC regions. The ratio depends on the relative scale height of GMCs, xi, and for xi values 0.1...0.75 we find the typical ratios of 0.6...1.1. The effective extinction law turns out to be very flat in GMC regions. We find the ratios of apparent extinctions of A(H)/A(K)=1.35...1.55 and A(J)/A(H)=1.15. The effect of the scattered flux on the effective reddening law, as well as on the effective extinction law, is significant. Regarding the GMC mass function, we find no correlation between the input and observed slopes of the mass functions. Rather, the observed slope reflects the parameter $\xi$ and the dynamical range of the mass function. We estimate that only a fraction of 10...20 % of the total mass of GMCs is recovered, if the observed color-excess values are transformed to masses using the Galactic reddening law. In the case of individual clouds the fraction can vary between ~0...50 %.Comment: 8 pages, 10 figures, accepted for publication in A&A. Added missing histograms in Fig.

Courts and coups in Fiji: the 2008 High Court judgment in Qarase v Bainimarama

AusAI

Epigallocatechin Gallate Modulates Microglia Phenotype to Suppress Pro-Inflammatory Signalling Cues and Inhibit Phagocytosis

Microglia are crucial players in the pathogenesis of late onset Alzheimer’s Disease (AD), with evidence for both deleterious and beneficial effects. Identifying interventions to modulate microglial responsiveness, to promote Amyloid β (Aβ) clearance, disrupt plaque formation, or to dampen excessive inflammation has therapeutic potential. Bioavailable flavonoids, such as the flavan 3-ols, are of interest due to their antioxidant, metal chelating, signalling and anti-inflammatory potential. Primary microglia were treated with a series of structurally related flavanol 3-ols to assess effects on phagocytosis, cytokine release and transcriptional responses by RNA sequencing. Data indicated that the extent of hydroxylation and the presence of the galloyl moiety were strong determinants of flavan 3-ol activity. Epigallocatechin gallate (EGCG) was the most effective flavan-3-ol tested and strongly inhibited phagocytosis of Aβ independent of any metal chelating properties, suggesting a more direct modulation of microglia responsiveness. EGCG was broadly anti-inflammatory, reducing cytokine release and downregulating transcription, particularly of components of the microglia extracellular matrix such as MMP3 and SerpinB2. Collectively, this brings new insight into the actions of flavonoids on microglial responsiveness with potential implications for the therapeutic use of EGCG and structurally related flavanol-3-ols in AD

Timescale analysis of a mathematical model of acetaminophen metabolism andtoxicity

Acetaminophen is a widespread and commonly used painkiller all over the world. However, it can cause liver damage when taken in large doses or at repeated chronic doses. Current models of acetaminophen metabolism are complex, and limited to numerical investigation though provide results that represent clinical investigation well. We derive a mathematical model based on mass action laws aimed at capturing the main dynamics of acetaminophen metabolism, in particular the contrast between normal and overdose cases, whilst remaining simple enough for detailed mathematical analysis that can identify key parameters and quantify their role in liver toxicity. We use singular perturbation analysis to separate the di fferent timescales describing the sequence of events in acetaminophen metabolism, systematically identifying which parameters dominate during each of the successive stages. Using this approach we determined, in terms of the model parameters, the critical dose between safe and overdose cases, timescales for exhaustion and regeneration of important cofactors for acetaminophen metabolism and total toxin accumulation as a fraction of initial dose

Age and Origin of Monazite Symplectite in an Iron Oxide-Apatite Deposit in the Adirondack Mountains, New York, USA: Implications for Tracking Fluid Conditions

Monazite crystals, intergrown with allanite, fluorapatite, and quartz from the Cheever Mine iron oxide-apatite (IOA-type) deposit in Essex County, New York, USA, display rare symplectite textures. Electron probe wavelength-dispersive spectrometry (WDS) mapping and major and trace element characterization of these features reveal a natural experiment in fluid-mediated monazite recrystallization. Two types of monazite with symplectite intergrowths have been recognized (Type I and II). Both types of symplectite development are associated with a decrease in HREE, Si, Ca, Th, and Y, but an increase in both La and Ce in monazite. Electron microprobe Th-U-total Pb analysis of Type I monazite with suitable ThO2 concentrations yielded a weighted mean age of 980 ± 5.8 Ma (MSWD: 3.3), which is interpreted as the age of monazite formation and the onset of symplectite development. Both types of monazite formed during a series of reactions from fluorapatite, and possibly britholite, to produce the final assemblage of monazite, allanite, and fluorapatite. Monazite formation was likely a response to evolving fluid conditions, which favored monazite stability over fluorapatite at ca. 980 Ma, possibly a NaCl brine. A subsequent transition to a Ca-dominated fluid may have then promoted the consumption of monazite to produce another generation of allanite and fluorapatite. Our results indicate that recrystallized monazite formed during fluid-mediated processes that, over time, trended towards an increasingly pure end-member composition. Regionally, these data are consistent with a magmatic-origin followed by fluid-mediated remobilization of select phases at subsolidus conditions for the Adirondack IOA deposits

Timescale analysis of a mathematical model of acetaminophen metabolism and toxicity

Acetaminophen is a widespread and commonly used painkiller all over the world. However, it can cause liver damage when taken in large doses or at repeated chronic doses. Current models of acetaminophen metabolism are complex, and limited to numerical investigation though provide results that represent clinical investigation well. We derive a mathematical model based on mass action laws aimed at capturing the main dynamics of acetaminophen metabolism, in particular the contrast between normal and overdose cases, whilst remaining simple enough for detailed mathematical analysis that can identify key parameters and quantify their role in liver toxicity. We use singular perturbation analysis to separate the different timescales describing the sequence of events in acetaminophen metabolism, systematically identifying which parameters dominate during each of the successive stages. Using this approach we determined, in terms of the model parameters, the critical dose between safe and overdose cases, timescales for exhaustion and regeneration of important cofactors for acetaminophen metabolism and total toxin accumulation as a fraction of initial dose

Lipid Bilayer thickness measured by quantitative DIC reveals phase transitions and effects of substrate hydrophilicity

Quantitative differential interference contrast microscopy is demonstrated here as a label-free method, which is able to image and measure the thickness of lipid bilayers with 0.1 nm precision. We investigate the influence of the substrate on the thickness of fluid-phase 1,2-dioleoyl-sn-glycero-3-phosphocholine (DOPC)-supported lipid bilayers and find a thinning of up to 10%, depending on substrate hydrophilicity, local bilayer coverage, and ionic strength of the medium. With fluorescently labeled lipid bilayers, we also observe changes in the bilayer thickness depending on the choice of fluorophore. Furthermore, liquid-ordered domains in bilayers, formed from DOPC, cholesterol, and sphingomyelin, are measured, and the corresponding thickness change between the liquid-ordered and liquid-disordered phases is accurately determined. Again, the thickness difference is found to be dependent on the presence of the fluorophore label, highlighting the need for quantitative label-free techniques

Why Wait?: Early Enteral Feeding After Pediatric Gastrostomy Tube Placement

Purpose Early initiation of feedings after gastrostomy tube (GT) placement may reduce associated hospital costs, but many surgeons fear complications could result from earlier feeds. We hypothesized that, irrespective of placement method, starting feedings within the first 6 h following GT placement would not result in a greater number of post-operative complications. Methods An IRB-approved retrospective review of all GTs placed between January 2012 and December 2014 at three academic institutions was undertaken. Data was stratified by placement method and whether the patient was initiated on feeds at less than 6 h or after. Baseline demographics, operative variables, post-operative management and complications were analyzed. Descriptive statistics were used and P-values < 0.05 were considered significant. Results One thousand and forty-eight patients met inclusion criteria. GTs were inserted endoscopically (48.9%), laparoscopically (44.9%), or via an open approach (6.2%). Demographics were similar in early and late fed groups. When controlling for method of placement, those patients who were fed within the first 6 h after gastrostomy placement had shorter lengths of stay compared to those fed greater than 6 h after placement (P < 0.05). Total post-operative outcomes were equivalent between feeding groups for all methods of placement (laparoscopic (P = 0.87), PEG (P = 0.94), open (P = 0.81)). Conclusions Early initiation of feedings following GT placement was not associated with an increase in complications. Feeds initiated earlier may shorten hospital stays and decrease overall hospital costs

Knockout of latrophilin-3 in Sprague-Dawley rats causes hyperactivity, hyper-reactivity, under-response to amphetamine, and disrupted dopamine markers

Attention deficit hyperactivity disorder is a pervasive developmental disorder characterized by inattention, impulsivity, and hyperactivity and is 75–90% heritable. Latrophilin-3 (LPHN3; or ADGRL(3)) is associated with a subtype of ADHD, but how it translates to symptoms is unknown. LPHN3 is a synaptic adhesion G protein coupled receptor that binds to fibronectin leucine rich transmembrane protein 3 and teneurin-3 (FLRT3 and TEN-3). We created a null mutation of Lphn3 (KO) in Sprague-Dawley rats using CRISPR/Cas9 to delete exon-3. The KO rats had no effects on reproduction or survival but reduced growth. KO females showed catch-up weight gain whereas KO males did not. We tested WT and KO littermates for home-cage activity, anxiety-like behavior, acoustic startle response, and activity after amphetamine challenge. Expression of Lphn3-related genes, monoamines, and receptors were determined. Lphn3 KO rats showed persistent hyperactivity, increased acoustic startle, reduced activity in response to amphetamine relative to baseline, and female-specific reduced anxiety-like behavior. Expression of Lphn1, Lphn2, and Flrt3 by qPCR and their protein products by western-blot analysis showed no compensatory upregulation. Striatal tyrosine hydroxylase, aromatic L-amino acid decarboxylase (AADC), and the dopamine transporter were increased and dopamine D1 receptor (DRD1) and dopamine- and cAMP-regulated neuronal phosphoprotein (DARPP-32) decreased with no changes in DRD2, DRD4, vesicular monoamine transporter-2, N-methyl-d-aspartate (NMDA)-NR1, -NR2A, or -NR2B. LPHN3 is expressed in many brain regions but its function is largely unknown. Data from human, mouse, zebrafish, Drosophila and our new Lphn3 KO rat data collectively show that its disruption is significantly correlated with hyperactivity and associated striatal changes in dopamine markers