Ultrafast nonlocal control of spontaneous emission

Solid-state cavity quantum electrodynamics systems will form scalable nodes of future quantum networks, allowing the storage, processing and retrieval of quantum bits, where a real-time control of the radiative interaction in the cavity is required to achieve high efficiency. We demonstrate here the dynamic molding of the vacuum field in a coupled-cavity system to achieve the ultrafast nonlocal modulation of spontaneous emission of quantum dots in photonic crystal cavities, on a timescale of ~200 ps, much faster than their natural radiative lifetimes. This opens the way to the ultrafast control of semiconductor-based cavity quantum electrodynamics systems for application in quantum interfaces and to a new class of ultrafast lasers based on nano-photonic cavities.Comment: 15 pages, 4 figure

Incomplete Inhibition of Sphingosine 1-Phosphate Lyase Modulates Immune System Function yet Prevents Early Lethality and Non-Lymphoid Lesions

BACKGROUND: S1PL is an aldehyde-lyase that irreversibly cleaves sphingosine 1-phosphate (S1P) in the terminal step of sphingolipid catabolism. Because S1P modulates a wide range of physiological processes, its concentration must be tightly regulated within both intracellular and extracellular environments. METHODOLOGY: In order to better understand the function of S1PL in this regulatory pathway, we assessed the in vivo effects of different levels of S1PL activity using knockout (KO) and humanized mouse models. PRINCIPAL FINDINGS: Our analysis showed that all S1PL-deficient genetic models in this study displayed lymphopenia, with sequestration of mature T cells in the thymus and lymph nodes. In addition to the lymphoid phenotypes, S1PL KO mice (S1PL(-/-)) also developed myeloid cell hyperplasia and significant lesions in the lung, heart, urinary tract, and bone, and had a markedly reduced life span. The humanized knock-in mice harboring one allele (S1PL(H/-)) or two alleles (S1PL(H/H)) of human S1PL expressed less than 10 and 20% of normal S1PL activity, respectively. This partial restoration of S1PL activity was sufficient to fully protect both humanized mouse lines from the lethal non-lymphoid lesions that developed in S1PL(-/-) mice, but failed to restore normal T-cell development and trafficking. Detailed analysis of T-cell compartments indicated that complete absence of S1PL affected both maturation/development and egress of mature T cells from the thymus, whereas low level S1PL activity affected T-cell egress more than differentiation. SIGNIFICANCE: These findings demonstrate that lymphocyte trafficking is particularly sensitive to variations in S1PL activity and suggest that there is a window in which partial inhibition of S1PL could produce therapeutic levels of immunosuppression without causing clinically significant S1P-related lesions in non-lymphoid target organs

A 28W -108.9dB/-102.2dB THD/THD+N Hybrid ΔΣ-PWM Class-D Audio Amplifier with 91% Peak Efficiency and Reduced EMI Emission

Class-D amplifiers are often used in high-power audio applications due to their high power efficiency. They typically employ pulse-width modulation (PWM) at a fixed carrier frequency, which may cause electromagnetic interference (EMI). Setting this frequency fPWM) below the AM band (535 to 1605kHz) helps mitigate this, but its harmonics still contain substantial energy and must be filtered out by bulky LC filters with low cut-off frequencies (fc = 20 to 40 kHz), significantly increasing system cost and size. Stability considerations also constrain the amplifier's unity-gain frequency to be &lt; mathrm{f} {mathrm{PWM}}/pi [1], compromising the audio-band loop gain required to suppress output-stage nonlinearity. Setting fPWM above the AM band helps increase fc and allows a higher loop gain [2]. However, this results in narrower pulses at higher power levels (higher modulation index), which cannot be faithfully produced by the output stage, thus exacerbating its non-linearity. Delta-sigma modulation (DeltaSigma M) has fixed pulse widths and does not suffer from these narrow-pulse artefacts. However, the out-of-band noise of 1bit modulators then requires larger LC filters. Moreover, high-order loop filters must be used to achieve sufficient SQNR, which then require additional techniques to maintain stability as the modulation range approaches 100% [3].</p

A 28-W, -102.2-dB THD+N Class-D Amplifier Using a Hybrid ΔΣM-PWM Scheme

This article presents a 28-W class-D amplifier for automotive applications. The combination of a high switching frequency and a hybrid multibit Δ Σ M-PWM scheme results in high linearity over a wide range of output power, as well as low AM-band EMI. As a result, only a small (150-kHz cutoff frequency), and thus low-cost, LC filter is needed to meet the CISPR-25 EMI average limit (150 kHz-30 MHz) with 10-dB margin. At 28-W output power, the proposed amplifier achieves 91% efficiency while driving a 4- Ω load from a 14.4-V supply. It attains a peak THD+N of 0.00077% (-102.2 dB) for a 1-kHz input signal. </p

A 28W -108.9dB/-102.2dB THD/THD+N Hybrid ΔΣ-PWM Class-D Audio Amplifier with 91% Peak Efficiency and Reduced EMI Emission

Class-D amplifiers are often used in high-power audio applications due to their high power efficiency. They typically employ pulse-width modulation (PWM) at a fixed carrier frequency, which may cause electromagnetic interference (EMI). Setting this frequency fPWM) below the AM band (535 to 1605kHz) helps mitigate this, but its harmonics still contain substantial energy and must be filtered out by bulky LC filters with low cut-off frequencies (fc = 20 to 40 kHz), significantly increasing system cost and size. Stability considerations also constrain the amplifier's unity-gain frequency to be &lt; mathrm{f} {mathrm{PWM}}/pi [1], compromising the audio-band loop gain required to suppress output-stage nonlinearity. Setting fPWM above the AM band helps increase fc and allows a higher loop gain [2]. However, this results in narrower pulses at higher power levels (higher modulation index), which cannot be faithfully produced by the output stage, thus exacerbating its non-linearity. Delta-sigma modulation (DeltaSigma M) has fixed pulse widths and does not suffer from these narrow-pulse artefacts. However, the out-of-band noise of 1bit modulators then requires larger LC filters. Moreover, high-order loop filters must be used to achieve sufficient SQNR, which then require additional techniques to maintain stability as the modulation range approaches 100% [3].Green Open Access added to TU Delft Institutional Repository ‘You share, we take care!’ – Taverne project https://www.openaccess.nl/en/you-share-we-take-care Otherwise as indicated in the copyright section: the publisher is the copyright holder of this work and the author uses the Dutch legislation to make this work public.Electronic InstrumentationMicroelectronic

A 28-W, -102.2-dB THD+N Class-D Amplifier Using a Hybrid ΔΣM-PWM Scheme

This article presents a 28-W class-D amplifier for automotive applications. The combination of a high switching frequency and a hybrid multibit Δ Σ M-PWM scheme results in high linearity over a wide range of output power, as well as low AM-band EMI. As a result, only a small (150-kHz cutoff frequency), and thus low-cost, LC filter is needed to meet the CISPR-25 EMI average limit (150 kHz-30 MHz) with 10-dB margin. At 28-W output power, the proposed amplifier achieves 91% efficiency while driving a 4- Ω load from a 14.4-V supply. It attains a peak THD+N of 0.00077% (-102.2 dB) for a 1-kHz input signal. Green Open Access added to TU Delft Institutional Repository ‘You share, we take care!’ – Taverne project https://www.openaccess.nl/en/you-share-we-take-care Otherwise as indicated in the copyright section: the publisher is the copyright holder of this work and the author uses the Dutch legislation to make this work public.Electronic InstrumentationMicroelectronic

Are pain coping strategies and neuropathic pain associated with a worse outcome after conservative treatment for Achilles tendinopathy?: A prospective cohort study

Objectives To analyse whether (1) passive or active pain coping strategies and (2) presence of neuropathic pain component influences the change of Achilles tendinopathy (AT) symptoms over a course of 24 weeks in conservatively-treated patients. Design Prospective cohort study. Methods Patients with clinically-diagnosed chronic midportion AT were conservatively treated. At baseline, the Pain Coping Inventory (PCI) was used to determine scores of coping, which consisted of two domains, active and passive (score ranging from 0 to 1; the higher, the more active or passive). Presence of neuropathic pain (PainDETECT questionnaire, −1 to 38 points) was categorized as (a) unlikely (≤12 points), (b) unclear (13–18 points) and (c) likely (≥19 points). The symptom severity was determined with the validated Victorian Institute of Sports Assessment-Achilles (VISA-A) questionnaire (0–100) at baseline, 6, 12 and 24 weeks. We analysed the correlation between (1) PCI and (2) PainDETECT baseline scores with change in VISA-A score using an adjusted Generalized Estimating Equations model. Results Of 80 included patients, 76 (95%) completed the 24-weeks follow-up. The mean VISA-A score (standard deviation) increased from 43 (16) points at baseline to 63 (23) points at 24 weeks. Patients had a mean (standard deviation) active coping score of 0.53 (0.13) and a passive score of 0.43 (0.10). Twelve patients (15%) had a likely neuropathic pain component. Active and passive coping mechanisms and presence of neuropathic pain did not influence the change in AT symptoms (p = 0.459, p = 0.478 and p = 0.420, respectively). Conclusions Contrary to widespread belief, coping strategy and presence of neuropathic pain are not associated with a worse clinical outcome in this homogeneous group of patients with clinically diagnosed AT

Deficiency or inhibition of oxygen sensor Phd1 induces hypoxia tolerance by reprogramming basal metabolism.

HIF prolyl hydroxylases (PHD1-3) are oxygen sensors that regulate the stability of the hypoxia-inducible factors (HIFs) in an oxygen-dependent manner. Here, we show that loss of Phd1 lowers oxygen consumption in skeletal muscle by reprogramming glucose metabolism from oxidative to more anaerobic ATP production through activation of a Pparalpha pathway. This metabolic adaptation to oxygen conservation impairs oxidative muscle performance in healthy conditions, but it provides acute protection of myofibers against lethal ischemia. Hypoxia tolerance is not due to HIF-dependent angiogenesis, erythropoiesis or vasodilation, but rather to reduced generation of oxidative stress, which allows Phd1-deficient myofibers to preserve mitochondrial respiration. Hypoxia tolerance relies primarily on Hif-2alpha and was not observed in heterozygous Phd2-deficient or homozygous Phd3-deficient mice. Of medical importance, conditional knockdown of Phd1 also rapidly induces hypoxia tolerance. These findings delineate a new role of Phd1 in hypoxia tolerance and offer new treatment perspectives for disorders characterized by oxidative stress