Sparsity driven ultrasound imaging

An image formation framework for ultrasound imaging from synthetic transducer arrays based on sparsity-driven regularization functionals using single-frequency Fourier domain data is proposed. The framework involves the use of a physics-based forward model of the ultrasound observation process, the formulation of image formation as the solution of an associated optimization problem, and the solution of that problem through efficient numerical algorithms. The sparsity-driven, model-based approach estimates a complex-valued reflectivity field and preserves physical features in the scene while suppressing spurious artifacts. It also provides robust reconstructions in the case of sparse and reduced observation apertures. The effectiveness of the proposed imaging strategy is demonstrated using experimental data

Stabilized lasers for advanced gravitational wave detectors

Second generation gravitational wave detectors require high power lasers with more than 100 W of output power and with very low temporal and spatial fluctuations. To achieve the demanding stability levels required, low noise techniques and adequate control actuators have to be part of the high power laser design. In addition feedback control and passive noise filtering is used to reduce the fluctuations in the so-called prestabilized laser system (PSL). In this paper, we discuss the design of a 200 W PSL which is under development for the Advanced LIGO gravitational wave detector and will present the first results. The PSL noise requirements for advanced gravitational wave detectors will be discussed in general and the stabilization scheme proposed for the Advanced LIGO PSL will be described

In situ uniaxial pressure cell for x-ray and neutron scattering experiments

We present an in situ uniaxial pressure device optimized for small angle x-ray and neutron scattering experiments at low-temperatures and high magnetic fields. A stepper motor generates force, which is transmitted to the sample via a rod with an integrated transducer that continuously monitors the force. The device has been designed to generate forces up to 200 N in both compressive and tensile configurations, and a feedback control allows operating the system in a continuous-pressure mode as the temperature is changed. The uniaxial pressure device can be used for various instruments and multiple cryostats through simple and exchangeable adapters. It is compatible with multiple sample holders, which can be easily changed depending on the sample properties and the desired experiment and allow rapid sample changes

The coactivator role of histone deacetylase 3 in IL-1-signaling involves deacetylation of p65 NF-kappaB

Histone deacetylase (HDAC) 3, as a cofactor in co-repressor complexes containing silencing mediator for retinoid or thyroid-hormone receptors (SMRT) and nuclear receptor co-repressor (N-CoR), has been shown to repress gene transcription in a variety of contexts. Here, we reveal a novel role for HDAC3 as a positive regulator of IL-1-induced gene expression. Various experimental approaches involving RNAi-mediated knockdown, conditional gene deletion or small molecule inhibitors indicate a positive role of HDAC3 for transcription of the majority of IL-1-induced human or murine genes. This effect was independent from the gene regulatory effects mediated by the broad-spectrum HDAC inhibitor trichostatin A (TSA) and thus suggests IL-1-specific functions for HDAC3. The stimulatory function of HDAC3 for inflammatory gene expression involves a mechanism that uses binding to NF-?B p65 and its deacetylation at various lysines. NF-?B p65-deficient cells stably reconstituted to express acetylation mimicking forms of p65 (p65 K/Q) had largely lost their potential to stimulate IL-1-triggered gene expression, implying that the co-activating property of HDAC3 involves the removal of inhibitory NF-?B p65 acetylations at K122, 123, 314 and 315. These data describe a novel function for HDAC3 as a co-activator in inflammatory signaling pathways and help to explain the anti-inflammatory effects frequently observed for HDAC inhibitors in (pre)clinical use

The coactivator role of histone deacetylase 3 in IL-1-signaling involves deacetylation of p65 NF-κB

Histone deacetylase (HDAC) 3, as a cofactor in co-repressor complexes containing silencing mediator for retinoid or thyroid-hormone receptors (SMRT) and nuclear receptor co-repressor (N-CoR), has been shown to repress gene transcription in a variety of contexts. Here, we reveal a novel role for HDAC3 as a positive regulator of IL-1-induced gene expression. Various experimental approaches involving RNAi-mediated knockdown, conditional gene deletion or small molecule inhibitors indicate a positive role of HDAC3 for transcription of the majority of IL-1-induced human or murine genes. This effect was independent from the gene regulatory effects mediated by the broad-spectrum HDAC inhibitor trichostatin A (TSA) and thus suggests IL-1-specific functions for HDAC3. The stimulatory function of HDAC3 for inflammatory gene expression involves a mechanism that uses binding to NF-κB p65 and its deacetylation at various lysines. NF-κB p65-deficient cells stably reconstituted to express acetylation mimicking forms of p65 (p65 K/Q) had largely lost their potential to stimulate IL-1-triggered gene expression, implying that the co-activating property of HDAC3 involves the removal of inhibitory NF-κB p65 acetylations at K122, 123, 314 and 315. These data describe a novel function for HDAC3 as a co-activator in inflammatory signaling pathways and help to explain the anti-inflammatory effects frequently observed for HDAC inhibitors in (pre)clinical us

In situ uniaxial pressure cell for x-ray and neutron scattering experiments

We present an in situ uniaxial pressure device optimized for small angle x-ray and neutron scattering experiments at low-temperatures and high magnetic fields. A stepper motor generates force, which is transmitted to the sample via a rod with an integrated transducer that continuously monitors the force. The device has been designed to generate forces up to 200 N in both compressive and tensile configurations, and a feedback control allows operating the system in a continuous-pressure mode as the temperature is changed. The uniaxial pressure device can be used for various instruments and multiple cryostats through simple and exchangeable adapters. It is compatible with multiple sample holders, which can be easily changed depending on the sample properties and the desired experiment and allow rapid sample changes

Serumproteinbindung von ACTH

3H- 1–23-Corticotropin wurde an Dextrangel (Sephadex G-25) gebunden und konnte durch Serumproteine, Albumin oder 0,1 N HCl eluiert werden. Mittels Dextrangelfiltration wurde gefunden, daß3H-ACTH kompetitiv an Serumproteine (Albumin) und Dextrangel gebunden wurde. Auch für natürliches Schweine-ACTH und endogenes ACTH in Patientenplasma (Adrenalektomie) wurde mittels biologischer ACTH-Bestimmung die Bindung von ACTH an Proteine bestätigt.3H- 1–23 corticotropin was bound to dextran gel (sephadex G-25) and was eluted by either serum proteins, albumin or 0.1 N HCl. Competitive binding of3H-ACTH to serum proteins (albumin) and dextran gel was shown by dextran gel filtration. Likewise natural ACTH (pig) and endogenous ACTH from plasma of an adrenalectomized patient were shown to be partly protein bound using biological ACTH-assay

Novel methodology for predicting the critical salt concentration of bubble coalescence inhibition

Bubble coalescence in some salt solutions can be inhibited if the salt concentration reaches a critical concentration Ccr. There are three models available for Ccr in the literature, but they fail to predict Ccr correctly. The first two models employ the van der Waals attraction power laws to establish Ccr from the discriminant of quadratic or cubic polynomials. To improve the two models, the third model uses the same momentum balance equation of the previous models but different intermolecular force generated by water hydration with exponential decaying. The third prediction for Ccr requires the experimental input for film rupture thickness and is incomplete. We show further in this paper that the third model is incorrect. We propose a novel methodology for determining C cr which resolves the mathematical uncertainties in modeling C cr and can explicitly predict it from any relevant intermolecular forces. The methodology is based on the discovery that Ccr occurs at the local maximum of the balance equation for the capillary pressure, disjoining pressure, and pressure of the Gibbs-Marangoni stress. The novel generic approach is successfully validated using nonlinear equations for complicated disjoining pressure

Distinct IL-1α-responsive enhancers promote acute and coordinated changes in chromatin topology in a hierarchical manner

How cytokine-driven changes in chromatin topology are converted into gene regulatory circuits during inflammation still remains unclear. Here, we show that interleukin (IL)-1α induces acute and widespread changes in chromatin accessibility via the TAK1 kinase and NF-κB at regions that are highly enriched for inflammatory disease-relevant SNPs. Two enhancers in the extended chemokine locus on human chromosome 4 regulate the IL-1α-inducible IL8 and CXCL1-3 genes. Both enhancers engage in dynamic spatial interactions with gene promoters in an IL-1α/TAK1-inducible manner. Microdeletions of p65-binding sites in either of the two enhancers impair NF-κB recruitment, suppress activation and biallelic transcription of the IL8/CXCL2 genes, and reshuffle higher-order chromatin interactions as judged by i4C interactome profiles. Notably, these findings support a dominant role of the IL8 “master” enhancer in the regulation of sustained IL-1α signaling, as well as for IL-8 and IL-6 secretion. CRISPR-guided transactivation of the IL8 locus or cross-TAD regulation by TNFα-responsive enhancers in a different model locus supports the existence of complex enhancer hierarchies in response to cytokine stimulation that prime and orchestrate proinflammatory chromatin responses downstream of NF-κB