Anderson Model out of equilibrium: decoherence effects in transport through a quantum dot

The paper deals with the nonequilibrium two-lead Anderson model, considered as an adequate description for transport through a d-c biased quantum dot. Using a self-consistent equation-of-motion method generalized out of equilibrium, we calculate a fourth-order decoherence rate $\gamma^{(4)}$ induced by a bias voltage $V$. This decoherence rate provides a cut-off to the infrared divergences of the self-energy showing up in the Kondo regime. At low temperature, the Kondo peak in the density of states is split into two peaks pinned at the chemical potential of the two leads. The height of these peaks is controlled by $\gamma^{(4)}$. The voltage dependence of the differential conductance exhibits a zero-bias peak followed by a broad Coulomb peak at large $V$, reflecting charge fluctuations inside the dot. The low-bias differential conductance is found to be a universal function of the normalized bias voltage $V/T_K$, where $T_K$ is the Kondo temperature. The universal scaling with a single energy scale $T_K$ at low bias voltages is also observed for the renormalized decoherence rate $\gamma^{(4)}/T_K$. We discuss the effect of $\gamma^{(4)}$ on the crossover from strong to weak coupling regime when either the temperature or the bias voltage is increased.Comment: 23 pages, 10 figure

How to move an amphipathic molecule across a lipid bilayer: different mechanisms for different ABC transporters?

Import of β-oxidation substrates into peroxisomes is mediated by ATP binding cassette (ABC) transporters belonging to subfamily D. In order to enter the β-oxidation pathway, fatty acids are activated by conversion to fatty acyl-CoA esters, a reaction which is catalysed by acyl-CoA synthetases (ACSs). Here, we present evidence for an unusual transport mechanism, in which fatty acyl-CoA substrates are accepted by ABC subclass D protein (ABCD) transporters, cleaved by the transporters during transit across the lipid bilayer to release CoA, and ultimately re-esterified in the peroxisome lumen by ACSs which interact with the transporter. We propose that this solves the biophysical problem of moving an amphipathic molecule across the peroxisomal membrane, since the intrinsic thioesterase activity of the transporter permits separate membrane translocation pathways for the hydrophobic fatty acid moiety and the polar CoA moiety. The cleavage/re-esterification mechanism also has the potential to control entry of disparate substrates into the β-oxidation pathway when coupled with distinct peroxisomal ACSs. A different solution to the movement of amphipathic molecules across a lipid bilayer is deployed by the bacterial lipid-linked oligosaccharide (LLO) flippase, PglK, in which the hydrophilic head group and the hydrophobic polyprenyl tail of the substrate are proposed to have distinct translocation pathways but are not chemically separated during transport. We discuss a speculative alternating access model for ABCD proteins based on the mammalian ABC transporter associated with antigen processing (TAP) and compare it to the novel mechanism suggested by the recent PglK crystal structures and biochemical data

A system for room acoustic simulation for one's own voice

The real-time simulation of room acoustical environments for one’s own voice, using generic software, has been difficult until very recently due to the computational load involved: requiring real-time convolution of a person’s voice with a potentially large number of long room impulse responses. This thesis is presenting a room acoustical simulation system with a software-based solution to perform real-time convolutions with headtracking; to simulate the effect of room acoustical environments on the sound of one’s own voice, using binaural technology. In order to gather data to implement headtracking in the system, human head- movements are characterized while reading a text aloud. The rooms that are simulated with the system are actual rooms that are characterized by measuring the room impulse response from the mouth to ears of the same head (oral binaural room impulse response, OBRIR). By repeating this process at 2o increments in the yaw angle on the horizontal plane, the rooms are binaurally scanned around a given position to obtain a collection of OBRIRs, which is then used by the software-based convolution system. In the rooms that are simulated with the system, a person equipped with a near- mouth microphone and near-ear loudspeakers can speak or sing, and hear their voice as it would sound in the measured rooms, while physically being in an anechoic room. By continually updating the person’s head orientation using headtracking, the corresponding OBRIR is chosen for convolution with their voice. The system described in this thesis achieves the low latency that is required to simulate nearby reflections, and it can perform convolution with long room impulse responses. The perceptual validity of the system is studied with two experiments, involving human participants reading aloud a set-text. The system presented in this thesis can be used to design experiments that study the various aspects of the auditory perception of the sound of one’s own voice in room environments. The system can also be adapted to incorporate a module that enables listening to the sound of one’s own voice in commercial applications such as architectural acoustic room simulation software, teleconferencing systems, virtual reality and gaming applications, etc

Mutagenesis separates ATPase and thioesterase activities of the peroxisomal ABC transporter, Comatose

The peroxisomal ABC transporter, Comatose (CTS), a full length transporter from Arabidopsis has intrinsic acyl-CoA thioesterase (ACOT) activity, important for physiological function. We used molecular modelling, mutagenesis and biochemical analysis to identify amino acid residues important for ACOT activity. D863, Q864 and T867 lie within transmembrane helix 9. These residues are orientated such that they might plausibly contribute to a catalytic triad similar to type II Hotdog fold thioesterases. When expressed in Saccharomyces cerevisiae, mutation of these residues to alanine resulted in defective of β-oxidation. All CTS mutants were expressed and targeted to peroxisomes and retained substrate-stimulated ATPase activity. When expressed in insect cell membranes, Q864A and S810N had similar ATPase activity to wild type but greatly reduced ACOT activity, whereas the Walker A mutant K487A had greatly reduced ATPase and no ATP-dependent ACOT activity. In wild type CTS, ATPase but not ACOT was stimulated by non-cleavable C14 ether-CoA. ACOT activity was stimulated by ATP but not by non-hydrolysable AMPPNP. Thus, ACOT activity depends on functional ATPase activity but not vice versa, and these two activities can be separated by mutagenesis. Whether D863, Q864 and T867 have a catalytic role or play a more indirect role in NBD-TMD communication is discussed

The arable ecosystem as battleground for emergence of new human pathogens

Disease incidences related to Escherichia coli and Salmonella enterica infections by consumption of (fresh) vegetables, sprouts, and occasionally fruits made clear that these pathogens are not only transmitted to humans via the “classical” routes of meat, eggs, and dairy products, but also can be transmitted to humans via plants or products derived from plants. Nowadays, it is of major concern that these human pathogens, especially the ones belonging to the taxonomical family of Enterobacteriaceae, become adapted to environmental habitats without losing their virulence to humans. Adaptation to the plant environment would lead to longer persistence in plants, increasing their chances on transmission to humans via consumption of plant-derived food. One of the mechanisms of adaptation to the plant environment in human pathogens, proposed in this paper, is horizontal transfer of genes from different microbial communities present in the arable ecosystem, like the ones originating from soil, animal digestive track systems (manure), water and plants themselves. Genes that would confer better adaptation to the phytosphere might be genes involved in plant colonization, stress resistance and nutrient acquisition and utilization. Because human pathogenic enterics often were prone to genetic exchanges via phages and conjugative plasmids, it was postulated that these genetic elements may be hold key responsible for horizontal gene transfers between human pathogens and indigenous microbes in agroproduction systems. In analogy to zoonosis, we coin the term phytonosis for a human pathogen that is transmitted via plants and not exclusively via animals

Variation-based design of an AM demodulator in a printed complementary organic technology

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Periprostatic fat measured on computed tomography as a marker for prostate cancer aggressiveness

Contains fulltext : 89797.pdf (publisher's version ) (Closed access)OBJECTIVE: Several reports found that obesity was associated with prostate cancer (PC) aggressiveness among men treated with radical prostatectomy or radiotherapy. Studies concerning this issue have basically relied on body mass index (BMI), as a marker for general obesity. Because visceral fat is the most metabolic active fat, we sought to evaluate if periprostatic fat measured on a computed tomography (CT) is a better marker than BMI to predict PC aggressiveness in a Dutch population who underwent brachytherapy for localized PC. PATIENTS AND METHODS: Of the 902 patients who underwent brachytherapy, 725 CT scans were available. Subcutaneous fat thickness (CFT), periprostatic fat area (cm(2)) and fat-density (%) were determined on the CT scan. Patients were stratified into three groups: 75 percentile of the fat-density. Associations between the three fat-density subgroups and BMI and PC aggressiveness were examined. RESULTS: 237 patients were classified as having normal weight (37.2%), 320 as overweight (50.2%) and 80 as obese (12.6%). There was a strong significant association between BMI and fat-density and CFT. The strongest correlation was seen between BMI and CFT (Pearson r coefficient = 0.71). Logistic regression analysis revealed no statistically significant association between the different fat measurements and the risk of having a high-risk disease. CONCLUSIONS: Periprostatic fat and fat-density as measured with CT were not correlated with PC aggressiveness in patients receiving brachytherapy. However, 31% of the patients with a normal BMI had a fat-density of >75 percentile of the periprostatic fat-density.01 december 201

Receiver Front-End Circuits for Future Generations of Wireless Communications

In this paper, new receiver concepts and CMOS circuits for future wireless communications standards are introduced. Tradeoffs between technology, performance and circuit choices of the RF front-end circuits are discussed. In particular, power consumption, noise figure and linearity trade-offs in low-noise amplifiers, mixers and oscillators are considered. The concepts derived are applied to a few classes of wireless communications standards that are broadband in nature at RF and/or require a broadband IF. Multi-mode, multi-band operation and adaptability as key requirements for future generation receivers are highlighted throughout the paper

ACBD5 deficiency causes a defect in peroxisomal very long-chain fatty acid metabolism

Background Acyl-CoA binding domain containing protein 5 (ACBD5) is a peroxisomal membrane protein with a cytosolic acyl-CoA binding domain. Because of its acyl-CoA binding domain, ACBD5 has been assumed to function as an intracellular carrier of acyl-CoA esters. In addition, a role for ACBD5 in pexophagy has been suggested. However, the precise role of ACBD5 in peroxisomal metabolism and/or functioning has not yet been established. Previously, a genetic ACBD5 deficiency was identified in three siblings with retinal dystrophy and white matter disease. We identified a pathogenic mutation in ACBD5 in another patient and studied the consequences of the ACBD5 defect in patient material and in ACBD5-deficient HeLa cells to uncover this role. Methods We studied a girl who presented with progressive leukodystrophy, syndromic cleft palate, ataxia and retinal dystrophy. We performed biochemical, cell biological and molecular studies in patient material and in ACBD5-deficient HeLa cells generated by CRISPR-Cas9 genome editing. Results We identified a homozygous deleterious indel mutation in ACBD5, leading to complete loss of ACBD5 protein in the patient. Our studies showed that ACBD5 deficiency leads to accumulation of very longchain fatty acids (VLCFAs) due to impaired peroxisomal beta-oxidation. No effect on pexophagy was found. Conclusions Our investigations strongly suggest that ACBD5 plays an important role in sequestering C26-CoA in the cytosol and thereby facilitates transport into the peroxisome and subsequent beta-oxidation. Accordingly, ACBD5 deficiency is a novel single peroxisomal enzyme deficiency caused by impaired VLCFA metabolism and leading to retinal dystrophy and white matter disease.Supported in part by funding through the Marie Curie Initial Training Networks (ITN) action to KDF, MS and HRW (FP7-2012-PERFUME-316723). MS is supported by the Biotechnology and Biological Sciences Research Council (BB/K006231/1; BB/N01541X/1)