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At least 595 records · Page 33

Fano interference at the excitation of coherent phonons: Relation between the asymmetry parameter and the initial phase of coherent oscillations

The theoretical assertion that the Fano asymmetry parameter and the asymptotic initial phase of a harmonic oscillator interacting with a continuum are interrelated is experimentally verified. By an example of coherent fully symmetric A{sub 1g} phonons in bismuth that are excited by ultrashort laser pulses at liquid helium temperature, it is demonstrated that, for negative values of the asymmetry parameter, the asymptotic phase increases as the modulus of the parameter decreases.

75 CONDENSED MATTER PHYSICS, SUPERCONDUCTIVITY AND↗

Energy Conservation in Distributed Interference as a Guarantee for Detecting a Detector Blinding Attack in Quantum Cryptography

An avalanche single-photon detector blinding attack is one of the methods for quantum hacking of quantum key distribution (QKD) systems. The attack was experimentally demonstrated for both phase- and polarization-encoded QKD systems. During this attack, an eavesdropper knows the entire key, does not produce errors and саnnot be detected. However, the phase encoding has neglected some significant features of the photocount statistics in the receiving party. It is shown in the paper at the level of fundamental principles that this attack changes the photocount statistics and leads to the detection of an eavesdropper. Expressions for the secret key length are obtained for this attack. This does not require any changes in the design and control electronics of the phase-encoded QKD system, and only changes in processing the results of registration of quantum states are sufficient. At the same time, the secret key vulnerability and compromise in polarization-encoded QKD systems is an existing fact rather than a potential menace.

71 CLASSICAL AND QUANTUM MECHANICS, GENERAL PHYSIC↗

Spin interference of holes in silicon nanosandwiches

Spin-dependent transport of holes is studied in silicon nanosandwiches on an n-Si (100) surface which are represented by ultranarrow p-Si quantum wells confined by {delta}-barriers heavily doped with boron. The measurement data of the longitudinal and Hall voltages as functions of the top gate voltage without an external magnetic field show the presence of edge conduction channels in the silicon nanosandwiches. An increase in the stabilized source-drain current within the range 0.25-5 nA subsequently exhibits the longitudinal conductance value 4e{sup 2}/h, caused by the contribution of the multiple Andreev reflection, the value 0.7(2e{sup 2}/h) corresponding to the known quantum conductance staircase feature, and displays Aharonov-Casher oscillations, which are indicative of the spin polarization of holes in the edge channels. In addition, at a low stabilized source-drain current, due to spin polarization, a nonzero Hall voltage is detected which is dependent on the top gate voltage; i. e., the quantum spin Hall effect is observed. The measured longitudinal I-V characteristics demonstrate Fiske steps and a negative differential resistance caused by the generation of electromagnetic radiation as a result of the Josephson effect. The results obtained are explained within a model of topological edge states which are a system of superconducting channels containing quantum point contacts transformable to single Josephson junctions at an increasing stabilized source-drain current.

36 MATERIALS SCIENCE↗

Ultrasonic Phased Array Evaluation of Control Rod Drive Mechanism (CRDM) Nozzle Interference Fit and Weld Region

In this investigation, non-destructive and destructive testing were used to evaluate potential boric acid leakage paths around an Alloy 600 CRDM penetration (Nozzle 63) from the North Anna Unit 2 reactor pressure vessel head that was removed from service in 2003. For this investigation, Nozzle 63 was examined using phased array ultrasonic testing. Prior to examining Nozzle 63, a CRDM penetration mockup with known notches and boric acid deposits was used to assess probe sensitivity, resolution and calibration. Following the non-destructive testing of Nozzle 63, the nozzle was destructively examined to visually assess the leak paths. These destructive and nondestructive results are compared and results are presented. The results of this investigation may be used by NRC to evaluate licensees’ volumetric leak path assessment methodologies and to support regulatory inspection requirements.

Ultrasonic, Phased Array, NDE, CRDM, Nozzle, Inter↗

Formation of iron complexs from trifluoroacetic acid based liquid chromatography mobile phases as interference ions in liquid chromatography/electrospray ionization mass spectrometric analysis

Two unexpected singly charged ions at m/z 1103 and 944 have been observed in mass spectra obtained from electrospray ionization-mass spectrometric analysis of liquid chromatography effluents with mobile phases containing trifluoroacetic acid. Accurate mass measurement and tandem mass spectrometry studies revealed that these two ions are not due to any contamination from solvents and chemicals used for mobile and stationary phases or from the laboratory atmospheric environment. Instead these ions are clusters of trifluoroacetic acid formed in association with acetonitrile, water and iron from the stainless steel union used to connect the column with the electrospray tip and to apply high voltage; the molecular formulae are Fe+((OH)(H2O)2)9(CF3COOH)5 and Fe+((OH)(H2O)2)6 (CF3COOH)5.

36 MATERIALS SCIENCE↗

Bounds on OPE coefficients from interference effects in the conformal collider

We apply the average null energy condition to obtain upper bounds on the three-point function coefficients of stress tensors and a scalar operator, ⟨TTO⟩, in general CFTs. We also constrain the gravitational anomaly of U(1) currents in four-dimensional CFTs, which are encoded in three-point functions of the form ⟨TTJ⟩. In theories with a large N AdS dual we translate these bounds into constraints on the coefficient of a higher derivative bulk term of the form ∫Φ W 2 . We speculate that these bounds also apply in de-Sitter. In this case our results constrain inflationary observables, such as the amplitude for chiral gravity waves that originate from higher derivative terms in the Lagrangian of the form Φ W W*.

72 PHYSICS OF ELEMENTARY PARTICLES AND FIELDS↗

Taking into Account Interelement Interference in X-Ray Fluorescence Analysis of Thin Two-Layer Ti/V Systems

We propose a new method for determining the thickness of layers in x-ray fluorescence analysis of two-layer Ti/V systems, using easily fabricated standardized film layers obtained by sputter deposition of titanium on a polymer film substrate. We have calculated correction factors taking into account the level of attenuation for the intensity of the primary emission from the x-ray tube and the analytical line for the element of the bottom layer in the top layer, and the enhancement of the fluorescence intensity for the top layer by the emission of atoms in the bottom layer.

37 INORGANIC, ORGANIC, PHYSICAL, AND ANALYTICAL CH↗

Proinsulin C-peptide interferes with insulin fibril formation

Highlights: Black-Right-Pointing-Pointer Insulin and C-peptide can interact under insulin fibril forming conditions. Black-Right-Pointing-Pointer C-peptide is incorporated into insulin aggregates and alters aggregation lag time. Black-Right-Pointing-Pointer C-peptide changes insulin fibril morphology and affects backbone accessibility. Black-Right-Pointing-Pointer C-peptide may be a regulator of fibril formation by {beta}-cell granule proteins. -- Abstract: Insulin aggregation can prevent rapid insulin uptake and cause localized amyloidosis in the treatment of type-1 diabetes. In this study, we investigated the effect of C-peptide, the 31-residue peptide cleaved from proinsulin, on insulin fibrillation at optimal conditions for fibrillation. This is at low pH and high concentration, when the fibrils formed are regular and extended. We report that C-peptide then modulates the insulin aggregation lag time and profoundly changes the fibril appearance, to rounded clumps of short fibrils, which, however, still are Thioflavine T-positive. Electrospray ionization mass spectrometry also indicates that C-peptide interacts with aggregating insulin and is incorporated into the aggregates. Hydrogen/deuterium exchange mass spectrometry further reveals reduced backbone accessibility in insulin aggregates formed in the presence of C-peptide. Combined, these effects are similar to those of C-peptide on islet amyloid polypeptide fibrillation and suggest that C-peptide has a general ability to interact with amyloidogenic proteins from pancreatic {beta}-cell granules. Considering the concentrations, these peptide interactions should be relevant also during physiological secretion, and even so at special sites post-secretory or under insulin treatment conditions in vivo.

60 APPLIED LIFE SCIENCES↗

Interference of silibinin with IGF-1R signalling pathways protects human epidermoid carcinoma A431 cells from UVB-induced apoptosis

Highlights: ► Silibinin protects A431 cells from UVB irradiation-induced apoptosis. ► Up-regulation of the IGF-1R-JNK/ERK pathways by UVB induces cell apoptosis. ► Silibinin inhibits IGF-1R pathways to repress caspase-8-mediated apoptosis. -- Abstract: Ultraviolet B (UVB) from sunlight is a major cause of cutaneous lesion. Silibinin, a traditional hepatic protectant, elicits protective effects against UVB-induced cellular damage. In A431 cells, the insulin-like growth factor-1 receptor (IGF-1R) was markedly up-regulated by UVB irradiation. The activation of the IGF-1R signalling pathways contributed to apoptosis of the cells rather than rescuing the cells from death. Up-regulated IGF-1R stimulated downstream mitogen-activated protein kinases (MAPKs), such as c-Jun N-terminal kinases (JNK) and extracellular signal-regulated protein kinases 1/2 (ERK1/2). The subsequent activation of caspase-8 and caspase-3 led to apoptosis. The activation of IGF-1R signalling pathways is the cause of A431 cell death. The pharmacological inhibitors and the small interfering RNA (siRNA) targeting IGF-1R suppressed the downstream activation of JNK/ERK-caspases to help the survival of the UVB-irradiated A431 cells. Indeed, silibinin treatment suppressed the IGF-1R-JNK/ERK pathways and thus protected the cells from UVB-induced apoptosis.

60 APPLIED LIFE SCIENCES↗

Liver X receptors interfere with the deleterious effect of diethylstilbestrol on testicular physiology

Highlights: • Part of the neonatal effect of DES on testis needs the presence of Lxrα/β. • Some DES-induced pathways are blocked in Lxr-deficient mice. • Lxr-deficient mice analysis defines DES-target genes protected by Lxr. - Abstract: Liver X receptors LXRα (NR1H3) and LXRβ (NR1H2) are transcription factors belonging to the nuclear receptor superfamily, activated by specific oxysterols, oxidized derivatives of cholesterol. These receptors are involved in the regulation of testis physiology. Lxr-deficient mice pointed to the physiological roles of these nuclear receptors in steroid synthesis, lipid homeostasis and germ cell apoptosis and proliferation. Diethylstilbestrol (DES) is a synthetic estrogen considered as an endocrine disruptor that affects the functions of the testis. Various lines of evidences have made a clear link between estrogens, their nuclear receptors ERα (NR3A1) and ERβ (NR3A2), and Lxrα/β. As LXR activity could also be regulated by the nuclear receptor small heterodimer partner (SHP, NR0A2) and DES could act through SHP, we wondered whether LXR could be targeted by estrogen-like endocrine disruptors such as DES. For that purpose, wild-type and Lxr-deficient mice were daily treated with 0.75 μg DES from days 1 to 5 after birth. The effects of DES were investigated at 10 or 45 days of age. We demonstrated that DES induced a decrease of the body mass at 10 days only in the Lxr-deficient mice suggesting a protective effect of Lxr. We defined three categories of DES-target genes in testis: those whose accumulation is independent of Lxr; those whose accumulation is enhanced by the lack of both Lxrα/β; those whose accumulation is repressed by the absence of Lxrα/β. Lipid accumulation is also modified by neonatal DES injection. Lxr-deficient mice present different lipid profiles, demonstrating that DES could have its effects in part due to Lxrα/β. Altogether, our study shows that both nuclear receptors Lxrα and Lxrβ are not only basally important for testicular physiology but could also have a preventive effect against estrogen-like endocrine disruptors.

60 APPLIED LIFE SCIENCES↗

Loss of zebrafish Smyd1a interferes with myofibrillar integrity without triggering the misfolded myosin response

Highlights: • Smyd1a is expressed in fast-twitch skeletal as well as heart muscle. • Loss-of smyd1b can be compensated by overexpression of smyd1a. • Smyd1a and smyd1b are part of different transcriptional regulatory mechanisms. Sarcomeric protein turnover needs to be tightly balanced to assure proper assembly and renewal of sarcomeric units within muscle tissues. The mechanisms regulating these fundamental processes are only poorly understood, but of great clinical importance since many cardiac and skeletal muscle diseases are associated with defective sarcomeric organization. The SET- and MYND domain containing protein 1b (Smyd1b) is known to play a crucial role in myofibrillogenesis by functionally interacting with the myosin chaperones Unc45b and Hsp90α1. In zebrafish, Smyd1b, Unc45b and Hsp90α1 are part of the misfolded myosin response (MMR), a regulatory transcriptional response that is activated by disturbed myosin homeostasis. Genome duplication in zebrafish led to a second smyd1 gene, termed smyd1a. Morpholino- and CRISPR/Cas9-mediated knockdown of smyd1a led to significant perturbations in sarcomere structure resulting in decreased cardiac as well as skeletal muscle function. Similar to Smyd1b, we found Smyd1a to localize to the sarcomeric M-band in skeletal and cardiac muscles. Overexpression of smyd1a efficiently compensated for the loss of Smyd1b in flatline (fla) mutant zebrafish embryos, rescued the myopathic phenotype and suppressed the MMR in Smyd1b-deficient embryos, suggesting overlapping functions of both Smyd1 paralogs. Interestingly, Smyd1a is not transcriptionally activated in Smyd1b-deficient fla mutants, demonstrating lack of genetic compensation despite the functional redundancy of both zebrafish Smyd1 paralogs.

60 APPLIED LIFE SCIENCES↗

Kinetic and structural evidence for specific DMSO interference with reversible binding of uncharged bis-oximes to hAChE and their reactivation kinetics of OP-hAChE

The structural basis of inhibitory effect of organic solvent dimethyl sulfoxide (DMSO) on human acetylcholinesterase (EC 3.1.1.7; hAChE) was inferred from the effect of DMSO on kinetics of reversible inhibition of uncharged, heterocyclic bis-oximes to hAChE, from DMSO effect on rates of reactivation of inactive organophosphate (OP)-hAChE conjugates by bis-oximes and by X-ray structures of bis-oxime and DMSO binding to hAChE. Here, the reversible inhibition constant of DMSO for hAChE in 0.1 M phosphate buffer pH 7.4 at 22 °C, was K i = (0.32 ± 0.04) % (or 45 ± 5 mM). The K i of the bis-oxime LG-703 for hAChE was 3.2-fold larger in 1 % DMSO, consistent with direct competition between LG-703 and DMSO. The X-ray structure of the LG-703∗hAChE complex (PDB ID: 6U3P) shows DMSO and LG-703 bound to individual hAChE monomers, LG-703 in the chain A and DMSO in the chain B. In the co-crystallization both small molecules were present at a similar excess over their corresponding K i values for hAChE (7.8-fold for DMSO and 6.5-fold for LG-703) and formation of two different complexes (DMSO∗hAChE and LG-703∗hAChE), in the same crystal, appears consistent with inhibition kinetics. Furthermore, rates of reactivation of paraoxon-inhibited hAChE (POX-hAChE) and of VX-hAChE by LG-703 and by a novel heterocyclic bis-oxime LG-1922 were reduced 2 – 3-fold in DMSO, consistent with observation of the active-center-bound DMSO molecules in the newly solved structure of the LG-1922∗POX-hAChE complex presented here and in our POX-hAChE structure (PDB ID: 8DT2) showing obstruction of the reactivator access to the conjugated P atom.

Acetylcholinesterase inhibition↗