Deep-ocean Bottom Pressure and Temperature Sensors Report: Methods and Data

This report documents ocean bottom pressure data collected from September 1983 to May 1985 in eleven deployments of pressure sensors under the Gulf Stream northeast of Cape Hatteras in depths of 3300 to 3900 m, as part of the Gulf Stream Dynamics Experiment. In past experiments, pressure sensors suitable for ocean depths have typically exhibited systematic drifts in calibration that seriously contaminate any observed periodicities longer than a few days. We used Digiquartz sensors (manufactured by Paroscientific, Inc.), because these sensors offered potentially much lower drift than other commercially available sensors. In these sensors, either a bellows or a Bourdon tube applies stress to an osciilating quartz-crystal beam, causing its oscillation frequency to vary. Several factors influence the amount of drift: bellows vs. Bourdon-tube construction, the applied pressure, the duration of deployment, and, for some sensors, high-pressure preconditioning in the lab. For the sensors deployed in the Gulf Stream, the total drift during deployments lasting from 3 to 12 months ranged from undetectable (≦0.01 dbar) to 0.20 to 0.50 dbar. About half of the total drift typically occurred within the first 6 days of deployment. We estimate the residual error in the final pressure records, after the dedrifting calculations, to be typically 0.02 dbar r.m.s. (or 0.06 dbar r.m.s.) if the first 6 days of the record are excluded (or included, respectively). This low drift-error opens many possibilities for studies that require knowledge of the low-frequency dynamic pressure signal in the deep ocean. Part I on Methods contains a short review of bottom pressure measurement in the deep ocean, a description of the sensors that we used, a discussion of their performance and drift relative to type of construction and prior pressurization history ( preconditioning ), and estimates of the accuracy of the dedrifted pressure records. In Part II of this report, the full data processing is described, including calibaration parameters, corrections for the influence of temperature variations on the pressure sensor, and parameterization to remove sendor drift errors by least-squares regression onto an exponentially decaying time-dependence. Time series are plotted which illustrate several steps in the processing: the edited half-hourly pressure records, the detided pressures with drift-model curves superimposed, and the low-pass filtered, dedrifted pressure records (i.e., after subtracting the estimated drift curve)

Analysis of a One-Dimensional Continuous Delay-Tolerant Network Model

The packet speed and transmission cost are examined, for a single packet traveling along a simple one-dimensional, continuous-time network, using a combination of wireless transmissions and physical transports. We assume that the network consists of two nodes moving at constant speed on a circle, and changing their direction of travel after independent exponential times. The packet wishes to travel in the clockwise direction as fast and as far as possible. It travels either by being physically transported on a node’s buffer, or by being wirelessly transmitted to the other node when the two are in the same location. We derive exact, explicit expressions for the long-term average packet speed (in the clockwise direction), and also for the average wireless transmission cost. These results can be viewed as initial steps towards the development of analogous exact expressions for the speed and cost, in more realistic, two-dimensional wireless delay-tolerant network models

A simple network of nodes moving on the circle

Two simple Markov processes are examined, one in discrete and one in continuous time, arising from idealized versions of a transmission protocol for mobile, delay-tolerant networks. We consider two independent walkers moving with constant speed on either the discrete or continuous circle, and changing directions at independent geometric (respectively, exponential) times. One of the walkers carries a message that wishes to travel as far and as fast as possible in the clockwise direction. The message stays with its current carrier unless the two walkers meet, the carrier is moving counter-clockwise, and the other walker is moving clockwise. In that case, the message jumps to the other walker. The long-term average clockwise speed of the message is computed. An explicit expression is derived via the solution of an associated boundary value problem in terms of the generator of the underlying Markov process. The average transmission cost is also similarly computed, measured as the long-term number of jumps the message makes per unit time. The tradeoff between speed and cost is examined, as a function of the underlying problem parameters

Thymocyte-specific truncation of the deubiquitinating domain of CYLD impairs positive selection in a NF-kappaB essential modulator-dependent manner

The cylindromatosis tumor suppressor gene (Cyld) encodes a deubiquitinating enzyme (CYLD) with immunoregulatory function. In this study, we evaluated the role of Cyld in T cell ontogeny by generating a mouse (Cyld(Delta9)) with a thymocyte-restricted Cyld mutation that causes a C-terminal truncation of the protein and reciprocates catalytically inactive human mutations. Mutant mice had dramatically reduced single positive thymocytes and a substantial loss of peripheral T cells. The analyses of polyclonal and TCR-restricted thymocyte populations possessing the mutation revealed a significant block in positive selection and an increased occurrence of apoptosis at the double-positive stage. Interestingly, in the context of MHC class I and II restricted TCR transgenes, lack of functional CYLD caused massive deletion of thymocytes that would have been positively selected, which is consistent with an impairment of positive selection. Biochemical analysis revealed that Cyld(Delta9) thymocytes exhibit abnormally elevated basal activity of NF-kappaB and JNK. Most importantly, inactivation of NF-kappaB essential modulator fully restored the NF-kappaB activity of Cyld(Delta9) thymocytes to physiologic levels and rescued their developmental and survival defect. This study identifies a fundamental role for functional CYLD in establishing the proper threshold of activation for thymocyte selection by a mechanism dependent on NF-kappaB essential modulator

Clumping Morphology Influences Virulence Uncoupled from Echinocandin Resistance in \u3cem\u3eCandida glabrata\u3c/em\u3e

Here, we report two paired sets of an index wild-type Candida glabrata bloodstream isolate and subsequent echinocandin-resistant FKS mutant. One paired set exhibited a higher proportion of clumping cells and was more virulent in the invertebrate host Galleria mellonella than the other paired set. No virulence difference between the paired index and FKS strains was observed. These findings imply a potential link of clumping morphology with virulence in C. glabrata that is uncoupled from FKS-mediated echinocandin resistance. IMPORTANCE Candida glabrata is a leading cause of invasive candidiasis. In contrast to other species, it has a high propensity for developing resistance to echinocandins, which are the first-line treatment. Unlike the dimorphic Candida albicans which can grow invasive filamentous hyphae, C. glabrata lacks this ability. Here, we report a link between virulence and clumping cell morphology in two different sets of clinical C. glabrata strains obtained from patients failing echinocandin therapy. One set of paired strains (echinocandin-susceptible and subsequent resistant mutant) had a high proportion of clumping cells in the population and were significantly more virulent than another set which had fewer clumping cells. Additionally, we corroborate that echinocandin resistance does not impart a significant fitness cost. Our findings suggest that clumping morphology may be an important but previously underestimated virulence factor for C. glabrata and also aid our understand for the high prevalence of resistance observed in this species

Two remarks on generalized entropy power inequalities

This note contributes to the understanding of generalized entropy power inequalities. Our main goal is to construct a counter-example regarding monotonicity and entropy comparison of weighted sums of independent identically distributed log-concave random variables. We also present a complex analogue of a recent dependent entropy power inequality of Hao and Jog, and give a very simple proof.Comment: arXiv:1811.00345 is split into 2 papers, with this being on

The effect of cigarette smoke exposure on the development of inflammation in lungs, gut and joints of TNFΔARE mice

The inflammatory cytokine TNF-alpha is a central mediator in many immune-mediated diseases, such as Crohn's disease (CD), spondyloarthritis (SpA) and chronic obstructive pulmonary disease (COPD). Epidemiologic studies have shown that cigarette smoking (CS) is a prominent common risk factor in these TNF-dependent diseases. We exposed TNF Delta ARE mice; in which a systemic TNF-alpha overexpression leads to the development of inflammation; to 2 or 4 weeks of air or CS. We investigated the effect of deregulated TNF expression on CS-induced pulmonary inflammation and the effect of CS exposure on the initiation and progression of gut and joint inflammation. Upon 2 weeks of CS exposure, inflammation in lungs of TNF Delta ARE mice was significantly aggravated. However, upon 4 weeks of CS-exposure, this aggravation was no longer observed. TNF Delta ARE mice have no increases in CD4+ and CD8+ T cells and a diminished neutrophil response in the lungs after 4 weeks of CS exposure. In the gut and joints of TNF Delta ARE mice, 2 or 4 weeks of CS exposure did not modulate the development of inflammation. In conclusion, CS exposure does not modulate gut and joint inflammation in TNF Delta ARE mice. The lung responses towards CS in TNF Delta ARE mice however depend on the duration of CS exposure

Prevalent mutator genotype identified in fungal pathogen Candida glabrata promotes multi-drug resistance.

The fungal pathogen Candida glabrata has emerged as a major health threat since it readily acquires resistance to multiple drug classes, including triazoles and/or echinocandins. Thus far, cellular mechanisms promoting the emergence of resistance to multiple drug classes have not been described in this organism. Here we demonstrate that a mutator phenotype caused by a mismatch repair defect is prevalent in C. glabrata clinical isolates. Strains carrying alterations in mismatch repair gene MSH2 exhibit a higher propensity to breakthrough antifungal treatment in vitro and in mouse models of colonization, and are recovered at a high rate (55% of all C. glabrata recovered) from patients. This genetic mechanism promotes the acquisition of resistance to multiple antifungals, at least partially explaining the elevated rates of triazole and multi-drug resistance associated with C. glabrata. We anticipate that identifying MSH2 defects in infecting strains may influence the management of patients on antifungal drug therapy

Exploration of synergistic and redundant information sharing in static and dynamical Gaussian systems

To fully characterize the information that two source variables carry about a third target variable, one must decompose the total information into redundant, unique, and synergistic components, i.e., obtain a partial information decomposition (PID). However, Shannon's theory of information does not provide formulas to fully determine these quantities. Several recent studies have begun addressing this. Some possible definitions for PID quantities have been proposed and some analyses have been carried out on systems composed of discrete variables. Here we present an in-depth analysis of PIDs on Gaussian systems, both static and dynamical. We show that, for a broad class of Gaussian systems, previously proposed PID formulas imply that (i) redundancy reduces to the minimum information provided by either source variable and hence is independent of correlation between sources, and (ii) synergy is the extra information contributed by the weaker source when the stronger source is known and can either increase or decrease with correlation between sources. We find that Gaussian systems frequently exhibit net synergy, i.e., the information carried jointly by both sources is greater than the sum of information carried by each source individually. Drawing from several explicit examples, we discuss the implications of these findings for measures of information transfer and information-based measures of complexity, both generally and within a neuroscience setting. Importantly, by providing independent formulas for synergy and redundancy applicable to continuous time-series data, we provide an approach to characterizing and quantifying information sharing amongst complex system variables

Development of a Corticosteroid-Immunosuppressed Mouse Model to Study the Pathogenesis and Therapy of Influenza-Associated Pulmonary Aspergillosis

Influenza-associated pulmonary aspergillosis (IAPA) is a feared complication in patients with influenza tracheobronchitis, especially those receiving corticosteroids. Herein, we established a novel IAPA mouse model with low-inoculum Aspergillus infection and compared outcomes in mice with and without cortisone acetate (CA) immunosuppression. CA was an independent predictor of increased morbidity/mortality in mice with IAPA. Early antifungal treatment with liposomal amphotericin B was pivotal to improve IAPA outcomes in CA-immunosuppressed mice, even after prior antiviral therapy with oseltamivir. In summary, our model recapitulates key clinical features of IAPA and provides a robust preclinical platform to study the pathogenesis and treatment of IAPA