Fluorescence correlation spectroscopy in thin films at reflecting substrates as a means to study nanoscale structure and dynamics at soft-matter interfaces

Structure and dynamics at soft-matter interfaces play an important role in nature and technical applications. Optical single-molecule investigations are non-invasive and capable to reveal heterogeneities at the nanoscale. In this work we develop an autocorrelation function (ACF) approach to retrieve tracer diffusion parameters obtained from fluorescence correlation spectroscopy (FCS) experiments in thin liquid films at reflecting substrates. This approach then is used to investigate structure and dynamics in 100 nm thick 8CB liquid crystal films on silicon wafers with five different oxide thicknesses. We find a different extension of the structural reorientation of 8CB at the solid-liquid interface for thin and for thick oxide. For the thin oxides, the perylenediimide tracer diffusion dynamics in general agrees with the hydrodynamic modeling using no-slip boundary conditions with only a small deviation close to the substrate, while a considerably stronger decrease of the interfacial tracer diffusion is found for the thick oxides.Comment: 8 figure

Condition-Based Monitoring on High-Precision Gearbox for Robotic Applications

This work presents a theoretical and experimental study regarding defect detection in a robotic gearbox using vibration signals in both cyclostationary and noncyclostationary conditions. The existing work focuses on inferring the health of the robot during operation with little regard toward the defective element of the components. This article illustrates the detection of specific element damage of a robotic gearbox during a robotic cycle based on domain knowledge and presents a novel data-driven method for asset health. This starts by studying the robotic gearbox, specifically its kinematics as a planetary 2-stage reduction gearbox to acquire the knowledge of the rotations of each component. The signals acquired from a test bench with four sensors undergo different acquisition methods and signal processing techniques to correlate the elements' frequencies. The work shows the detection of the artificially created defects from the acquired vibration data, verifying the kinematic methodology and identifying the root cause of failure of such gearboxes. A novel resampling method, Binning, is presented and compared with the traditional signal processing techniques. Binning combined with Principal Component Analysis (PCA) as a data-driven method to infer the state of the gearbox is presented, tested, and validated. This work presents methods as a step toward automatized predictive maintenance on robots in industrial applications

Quasi-one-dimensional anisotropic Heisenberg model in a transverse magnetic field

The phase diagram of weakly coupled $XXZ$ chains in a transverse magnetic field is studied using the mean-field approximation for the interchain coupling and known exact results for an effective one-dimensional model. Results are applied to the quasi-one-dimensional antiferromagnet $Cs_{2}CoCl_{4}$ and the value of interchain interaction in this compound is estimated.Comment: 4 pages, 2 figure

Sodium nitroglycerin induces middle cerebral artery vasodilatation in young, healthy adults

© 2018 The Authors Experimental Physiology published by John Wiley & Sons Ltd on behalf of The Physiological Society New Findings: What is the central question of this study? Nitric oxide causes dilatation in peripheral vessels; however, whether nitric oxide affects basal cerebral artery dilatation has not been explored. What is the main finding and its importance? This study demonstrated that vasodilatation occurs in the right middle cerebral artery in response to exogenous nitric oxide. However, blood velocity decreased and, therefore, overall cerebral blood flow remained unchanged. This study provides new insight into the role of nitric oxide in cerebral blood flow control. Abstract: Recent evidence indicates that basal cerebral conduit vessels dilate with hypercapnia, with a nitric oxide (NO) mechanism explaining one way in which parenchymal cerebral arterioles dilate. However, whether NO affects basal cerebral artery dilatation remains unknown. This study quantified the effect of an exogenous NO donor [sodium nitroglycerin (NTG); 0.4 mg sublingual spray] on the right middle cerebral artery (rMCA) cross-sectional area (CSA), blood velocity and overall blood flow. Measures of vessel CSA (7 T magnetic resonance imaging) and MCA blood velocity (transcranial Doppler ultrasound) were made at baseline (BL) and after exogenous NTG or placebo (PLO) administration in young, healthy individuals (n = 10, two males, age range 20–23 years). The CSA increased in the rMCA [BL, 5.2 ± 1.2 mm2; PLO, 5.4 ± 1.5 mm2; NTG, 6.6 ± 1.5 mm2, P \u3c 0.05; mean ± SD]. Concurrently, rMCA blood velocity decreased from BL during NTG compared with PLO (BL, 67 ± 10 cm s−1; PLO, 62 ± 10 cm s−1; NTG, 59 ± 9.3 cm s−1, P \u3c 0.05; mean ± SD]. However, total MCA blood flow did not change with NTG or PLO [BL, 221 ± 37.4 ml min−1; PLO, 218 ± 35.0 ml min−1; NTG, 213 ± 46.4 ml min−1). Therefore, exogenous NO mediates a dilatory response in the rMCA, but not in its downstream vascular bed

Finite-Temperature Charge-Ordering Transition and Fluctuation Effects in Quasi-One-Dimensional Electron Systems at Quarter Filling

Finite-temperature charge-ordering phase transition in quasi one-dimensional (1D) molecular conductors is investigated theoretically, based on a quasi 1D extended Hubbard model at quarter filling with interchain Coulomb repulsion $V_\perp$. The interchain term is treated within mean-field approximation whereas the 1D fluctuations in the chains are fully taken into account by the bosonization theory. Three regions are found depending on how the charge ordered state appears at finite temperature when $V_\perp$ is introduced: (i) weak-coupling region where the system transforms from a metal to a charge ordered insulator with finite transition temperature at a finite critical value of $V_\perp$, (ii) an intermediate region where this transition occurs by infinitesimal $V_\perp$ due to the stability of inherent 1D fluctuation, and (iii) strong-coupling region where the charge ordered state is realized already in the purely 1D case, of which the transition temperature becomes finite with infinitesimal $V_\perp$. Analytical formula for the $V_\perp$ dependence of the transition temperature is derived for each region.Comment: 4 pages, submitted to J. Phys. Soc. Jp

Patients with adenosine deaminase deficiency surviving after hematopoietic stem cell transplantation are at high risk of CNS complications

Adenosine deaminase (ADA) deficiency is a systemic metabolic disease that causes an autosomal recessive variant of severe combined immunodeficiency (SCID) and less consistently other complications including neurologic abnormalities. Hematopoietic stem cell transplantation (HSCT) is able to correct the immunodeficiency, whereas control of nonimmunologic complications has not been extensively explored. We applied HSCT in 15 ADA-deficient patients consecutively treated at our institutions since 1982 and analyzed long-term outcome. Seven patients received transplants without conditioning from HLA-matched family donors (MFDs); the other 8 patients received conditioning and were given transplants either from HLA-mismatched family donors (MMFDs; n = 6) or from matched unrelated donors (MUDs; n = 2). At a mean follow-up period of 12 years (range, 4-22 years), 12 patients are alive with stable and complete immune reconstitution (7 of 7 after MFD, 4 of 6 after MMFD, and 1 of 2 after MUD transplantation). Six of 12 surviving patients show marked neurologic abnormalities, which include mental retardation, motor dysfunction, and sensorineural hearing deficit. We were unable to identify disease or transplantation-related factors correlating with this divergent neurologic outcome. The high rate of neurologic abnormalities observed in long-term surviving patients with ADA deficiency indicates that HSCT commonly fails to control CNS complications in this metabolic disease

Seasonality of biological and physical controls on surface ocean CO2 from hourly observations at the Southern Ocean Time Series site south of Australia

The Subantarctic Zone (SAZ), which covers the northern half of the Southern Ocean between the Subtropical and Subantarctic Fronts, is important for air-sea CO2 exchange, ventilation of the lower thermocline, and nutrient supply for global ocean productivity. Here we present the first high-resolution autonomous observations of mixed layer CO2 partial pressure (pCO(2)) and hydrographic properties covering a full annual cycle in the SAZ. The amplitude of the seasonal cycle in pCO(2) (similar to 60 mu atm), from near-atmospheric equilibrium in late winter to similar to 330 mu atm in midsummer, results from opposing physical and biological drivers. Decomposing these contributions demonstrates that the biological control on pCO(2) (up to 100 mu atm), is 4 times larger than the thermal component and driven by annual net community production of 2.45 +/- 1.47 mol C m(-2) yr(-1). After the summer biological pCO(2) depletion, the return to near-atmospheric equilibrium proceeds slowly, driven in part by autumn entrainment into a deepening mixed layer and achieving full equilibration in late winter and early spring as respiration and advection complete the annual cycle. The shutdown of winter convection and associated mixed layer shoaling proceeds intermittently, appearing to frustrate the initiation of production. Horizontal processes, identified from salinity anomalies, are associated with biological pCO(2) signatures but with differing impacts in winter (when they reflect far-field variations in dissolved inorganic carbon and/or biomass) and summer (when they suggest promotion of local production by the relief of silicic acid or iron limitation). These results provide clarity on SAZ seasonal carbon cycling and demonstrate that the magnitude of the seasonal pCO(2) cycle is twice as large as that in the subarctic high-nutrient, low-chlorophyll waters, which can inform the selection of optimal global models in this region

Seasonal modulation of mesoscale processes alters nutrient availability and plankton communities in the Red Sea

Hydrographic and atmospheric forcing set fundamental constraints on the biogeochemistry of aquatic ecosystems and manifest in the patterns of nutrient availability and recycling, species composition of communities, trophic dynamics, and ecosystem metabolism. In the Red Sea, latitudinal gradients in environmental conditions and primary production have been ascribed to fluctuations in Gulf of Aden Water inflow, upwelling/mixing, and regenerated nutrient utilization i.e. rapidly recycled nitrogen in upper layers. However, our understanding of upper layer dynamics and related changes in plankton communities, metabolism and carbon and nitrogen export is limited. We surmised that stratification and mesoscale eddies modulate the nutrient availability and taxonomic identity of plankton communities in the Red Sea. Based on remote-sensing data of sea level anomalies and high resolution in situ measurements (ScanFish) we selected stations for hydrographic CTD profiles, water sampling (nutrients, seawater oxygen stable isotopes [δ18OSW]), phytoplankton and zooplankton collections. In fall 2014, strong stratification subjected the plankton community to an overall nitrogen and phosphorus shortage. The nutrient deficiency increased numbers of heterotrophic dinoflagellates, microzooplankton, and diazotrophs (Trichodesmium, diatom-diazotroph associations [DDAs]), albeit largely decreased phytoplankton and mesozooplankton abundances. In spring 2015, mesoscale eddies increased the nutrient availability, and the thermohaline characteristics and low δ18OSW point to the interaction of eddies with Gulf of Aden Surface Water (GASW). Cyclonic eddies and, most likely, the availability of nutrients associated with the GASW, increased the abundances of autotrophs (diatoms, Prasinophytes) and supported larger numbers of zooplankton and their larvae. We demonstrate that the interplay of stratification, advection of Gulf of Aden water and mesoscale eddies are key elements to better understand changes in plankton community composition, ecosystem metabolism, and macronutrient export in the Red Sea in space and time

Prolonged treatment with pimelic o-aminobenzamide HDAC inhibitors ameliorates the disease phenotype of a Friedreich ataxia mouse model

NOTICE: this is the author’s version of a work that was accepted for publication in Neurobiology of Disease. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication.Friedreich ataxia (FRDA) is an inherited neurodegenerative disorder caused by GAA repeat expansion within the FXN gene, leading to epigenetic changes and heterochromatin-mediated gene silencing that result in a frataxin protein deficit. Histone deacetylase (HDAC) inhibitors, including pimelic o-aminobenzamide compounds 106, 109 and 136, have previously been shown to reverse FXN gene silencing in short-term studies of FRDA patient cells and a knock-in mouse model, but the functional consequences of such therapeutic intervention have thus far not been described. We have now investigated the long-term therapeutic effects of 106, 109 and 136 in our GAA repeat expansion mutation-containing YG8R FRDA mouse model. We show that there is no overt toxicity up to 5 months of treatment and there is amelioration of the FRDA-like disease phenotype. Thus, while the neurological deficits of this model are mild, 109 and 106 both produced an improvement of motor coordination, whereas 109 and 136 produced increased locomotor activity. All three compounds increased global histone H3 and H4 acetylation of brain tissue, but only 109 significantly increased acetylation of specific histone residues at the FXN locus. Effects on FXN mRNA expression in CNS tissues were modest, but 109 significantly increased frataxin protein expression in brain tissue. 109 also produced significant increases in brain aconitase enzyme activity, together with reduction of neuronal pathology of the dorsal root ganglia (DRG). Overall, these results support further assessment of HDAC inhibitors for treatment of Friedreich ataxia.This work was supported by Repligen Corporation; Muscular Dystrophy Association (MDA) USA; Ataxia UK; Friedreich's Ataxia Research Alliance (FARA); GoFAR; and the Wellcome Trust [089757]