Young LMC clusters: the role of red supergiants and multiple stellar populations in their integrated light and CMDs

The optical integrated spectra of three LMC young stellar clusters (NGC 1984, NGC 1994 and NGC 2011) exhibit concave continua and prominent molecular bands which deviate significantly from the predictions of single stellar population (SSP) models. In order to understand the appearance of these spectra, we create a set of young stellar population (MILES) models, which we make available to the community. We use archival International Ultraviolet Explorer integrated UV spectra to independently constrain the cluster masses and extinction, and rule out strong stochastic effects in the optical spectra. In addition, we also analyze deep colour-magnitude diagrams of the clusters to provide independent age determinations based on isochrone fitting. We explore hypotheses including age-spreads in the clusters, a top-heavy initial mass function, different SSP models and the role of red supergiant stars (RSG). We find that the strong molecular features in the optical spectra can only be reproduced by modeling an increased fraction of about 20 per cent by luminosity of RSG above what is predicted by canonical stellar evolution models. Given the uncertainties in stellar evolution at Myr ages, we cannot presently rule-out the presence of Myr age-spreads in these clusters. Our work combines different wavelengths as well as different approaches (resolved data as well as integrated spectra for the same sample) in order to reveal the complete picture. We show that each approach provides important information but in combination can we better understand the cluster stellar populations.Comment: Accepted for publication in MNRA

Neurosyphilis Masquerading as an Acute Adie's Tonic Pupil: Report of a Case

We describe the case of a male patient who presented with anisocoria, and was initially diagnosed with an acute Adie’s tonic pupil. On subsequent laboratory testing, he was found to have neurosyphilis. Magnetic resonance imaging demonstrated enhancement of the right oculomotor nerve. This case underscores the importance of considering this diagnosis in patients with acute onset internal ophthalmoplegia and hypersensitivity to dilute pilocarpine, even in the absence of other oculomotor nerve findings

Protein Kinase C inhibition ameliorates functional endothelial insulin resistance and Vascular Smooth Muscle Cell hypersensitivity to insulin in diabetic hypertensive rats

<p>Abstract</p> <p>Objective</p> <p>Insulin resistance, diabetes, and hypertension are considered elements of metabolic syndrome which is associated with vascular dysfunction. We investigated whether inhibition of protein kinase C (PKC) would affect vascular function in diabetic hypertensive (DH) rats.</p> <p>Methods</p> <p>A combination of type 2 diabetes and arterial hypertension was produced in male Sprague Dawley rats by intrauterine protein deprivation (IUPD) followed by high salt diet. At the age of 32 weeks, DH rats were treated for 2 weeks with the angiotensin-converting enzyme inhibitor captopril (Capto, 30 mg/kg), PKC inhibitor ruboxistaurin (RBX, 50 mg/kg) or vehicle (n = 8 per group) and blood pressure was monitored using telemetry. At the end of experiments, femoral arteries were dissected, and vascular reactivity was evaluated with isovolumic myography.</p> <p>Results</p> <p>The IUPD followed by high salt diet resulted in significant elevation of plasma glucose, plasma insulin, and blood pressure. Endothelium-dependent vascular relaxation in response to acetylcholine was blunted while vascular contraction in response to phenylephrine was enhanced in the DH rats. Neither Capto nor RBX restored endothelium-dependent vascular relaxation while both suppressed vascular contraction. Ex-vivo incubation of femoral arteries from control rats with insulin induced dose-response vasorelaxation while insulin failed to induce vasorelaxation in the DH rat arteries. In the control arteries treated with endothelial nitric oxide synthase inhibitor L-NAME, insulin induced vasoconstriction that was exacerbated in DH rats. Capto and RBX partially inhibited insulin-stimulated vascular contraction.</p> <p>Conclusion</p> <p>These findings suggest that PKC inhibition ameliorates functional endothelial insulin resistance and smooth muscle cell hypersensitivity to insulin, but does not restore acetylcholine-activated endothelium-dependent vasodilation in DH rats.</p

Geometry of River Networks II: Distributions of Component Size and Number

The structure of a river network may be seen as a discrete set of nested sub-networks built out of individual stream segments. These network components are assigned an integral stream order via a hierarchical and discrete ordering method. Exponential relationships, known as Horton's laws, between stream order and ensemble-averaged quantities pertaining to network components are observed. We extend these observations to incorporate fluctuations and all higher moments by developing functional relationships between distributions. The relationships determined are drawn from a combination of theoretical analysis, analysis of real river networks including the Mississippi, Amazon and Nile, and numerical simulations on a model of directed, random networks. Underlying distributions of stream segment lengths are identified as exponential. Combinations of these distributions form single-humped distributions with exponential tails, the sums of which are in turn shown to give power law distributions of stream lengths. Distributions of basin area and stream segment frequency are also addressed. The calculations identify a single length-scale as a measure of size fluctuations in network components. This article is the second in a series of three addressing the geometry of river networks.Comment: 16 pages, 13 figures, 4 tables, Revtex4, submitted to PR

Effect of Depth of Total Intravenous General Anesthesia on Intraoperative Electrically Evoked Compound Action Potentials in Cochlear Implantation Surgery.

PURPOSE: This study aims to compare the effect of the depth of total intravenous anesthesia (TIVA) on intraoperative electrically evoked compound action potential (e-ECAP) thresholds in cochlear implant operations. METHODS: Prospectively, a total of 39 patients aged between 1 and 48 years who were scheduled to undergo cochlear implantation surgeries were enrolled in this study. Every patient received both light and deep TIVA during the cochlear implant surgery. The e-ECAP thresholds were obtained during the light and deep TIVA. RESULTS: After comparing the e-ECAP means for each electrode (lead) between the light and deep anesthesia, no significant differences were detected between the light and deep anesthesia. CONCLUSION: The depth of TIVA may have no significant influence on the e-ECAP thresholds as there was no statistical difference between the light and deep anesthesia

Two-in-one aortic valve sizing and valvuloplasty conductance balloon catheter

BACKGROUND: Inaccurate aortic valve sizing and selection is linked to paravalvular leakage in transcatheter aortic valve replacement (TAVR). Here, a novel sizing valvuloplasty conductance balloon (SVCB) catheter is shown to be accurate, reproducible, unbiased, and provides real-time tool for aortic valve sizing that fits within the standard valvuloplasty procedure. METHODS AND RESULTS: The SVCB catheter is a valvuloplasty device that uses real-time electrical conductance measurements based on Ohm's Law to size the balloon opposed against the aortic valve at any given inflation pressure. Accuracy and repeatability of the SVCB catheter was performed on the bench in phantoms of known dimension and ex vivo in three domestic swine aortic annuli with comparison to computed tomography (CT) and dilator measurements. Procedural workflow and safety was demonstrated in vivo in three additional domestic swine. SVCB catheter measurements had negligible bias or error for bench accuracy considered as the gold standard (Bias: -0.11 ± 0.26 mm; Error: 1.2%), but greater disagreement in ex vivo versus dilators (Bias: -0.3 ± 1.1 mm; Error: 4.5%), and ex vivo versus CT (Bias: -1.0 ± 1.6 mm; Error: 8.7%). The dilator versus CT accuracy showed similar agreement (Bias: -0.9 ± 1.5 mm; Error: 7.3%). Repeatability was excellent on the bench (Bias: 0.02 ± 0.12 mm; Error: 0.5%) and ex vivo (Bias: -0.4 ± 0.9 mm; Error: 4.6%). In animal studies, the device fit well within the procedural workflow with no adverse events or complications. CONCLUSIONS: Due to the clinical relevance of this accurate, repeatable, unbiased, and real-time sizing measurement, the SVCB catheter may provide a useful tool prior to TAVR. These findings merit a future human study

Regulation of 130kDa smooth muscle myosin light chain kinase expression by an intronic CArG element

The mylk1 gene encodes a 220-kDa nonmuscle myosin light chain kinase (MLCK), a 130-kDa smooth muscle MLCK (smMLCK), as well as the non-catalytic product telokin. Together, these proteins play critical roles in regulating smooth muscle contractility. Changes in their expression are associated with many pathological conditions; thus, it is important to understand the mechanisms regulating expression of mylk1 gene transcripts. Previously, we reported a highly conserved CArG box, which binds serum response factor, in intron 15 of mylk1. Because this CArG element is near the promoter that drives transcription of the 130-kDa smMLCK, we examined its role in regulating expression of this transcript. Results show that deletion of the intronic CArG region from a β-galactosidase reporter gene abolished transgene expression in mice in vivo. Deletion of the CArG region from the endogenous mylk1 gene, specifically in smooth muscle cells, decreased expression of the 130-kDa smMLCK by 40% without affecting expression of the 220-kDa MLCK or telokin. This reduction in 130-kDa smMLCK expression resulted in decreased phosphorylation of myosin light chains, attenuated smooth muscle contractility, and a 24% decrease in small intestine length that was associated with a significant reduction of Ki67-positive smooth muscle cells. Overall, these data show that the CArG element in intron 15 of the mylk1 gene is necessary for maximal expression of the 130-kDa smMLCK and that the 130-kDa smMLCK isoform is specifically required to regulate smooth muscle contractility and small intestine smooth muscle cell proliferation