Deterministic coupling of a single silicon-vacancy color center to a photonic crystal cavity in diamond

Deterministic coupling of single solid-state emitters to nanocavities is the key for integrated quantum information devices. We here fabricate a photonic crystal cavity around a preselected single silicon-vacancy color center in diamond and demonstrate modification of the emitters internal population dynamics and radiative quantum efficiency. The controlled, room-temperature cavity coupling gives rise to a resonant Purcell enhancement of the zero-phonon transition by a factor of 19, coming along with a 2.5-fold reduction of the emitter's lifetime

Evaluation of nitrogen- and silicon-vacancy defect centres as single photon sources in quantum key distribution

We demonstrate a quantum key distribution (QKD) testbed for room temperature single photon sources based on defect centres in diamond. A BB84 protocol over a short free-space transmission line is implemented. The performance of nitrogen-vacancy (NV) as well as silicon-vacancy defect (SiV) centres is evaluated and an extrapolation for next-generation sources with enhanced efficiency is discussed.Comment: 14 pages, 5 figure

Visible-to-telecom quantum frequency conversion of light from a single quantum emitter

Quantum frequency conversion (QFC), a nonlinear optical process in which the frequency of a quantum light field is altered while conserving its non-classical correlations, was first demonstrated 20 years ago. Meanwhile, it is considered an essential tool for the implementation of quantum repeaters since it allows for interfacing quantum memories with telecom-wavelength photons as quantum information carriers. Here we demonstrate efficient (>30%) QFC of visible single photons (711 nm) emitted by a quantum dot (QD) to a telecom wavelength (1,313 nm). Analysis of the first and second-order coherence before and after wavelength conversion clearly proves that important properties, such as the coherence time and photon antibunching, are fully conserved during the frequency translation process. Our findings underline the great potential of single photon sources on demand in combination with QFC as a promising technique for quantum repeater schemes.Comment: 11 pages, 4 figure

Differential Expression of Matrix Metalloproteases in Human Fibroblasts with Different Origins

Fibroblasts are widely distributed cells and are responsible for the deposition of extracellular matrix (ECM) components but also secrete ECM-degrading matrix metalloproteases. A finely balanced equilibrium between deposition and degradation of ECM is essential for structural integrity of tissues. In the past, fibroblasts have typically been understood as a uniform cell population with comparable functions regardless of their origin. Here, we determined growth curves of fibroblasts derived from heart, skin, and lung and clearly show the lowest proliferation rate for cardiac fibroblasts. Furthermore, we examined basal expression levels of collagen and different MMPs in these three types of fibroblasts and compared these concerning their site of origin. Interestingly, we found major differences in basal mRNA expression especially for MMP1 and MMP3. Moreover, we treated fibroblasts with TNF-α and observed different alterations under these proinflammatory conditions. In conclusion, fibroblasts show different properties in proliferation and MMP expression regarding their originated tissue

Decrease in the expression of the type 1 PTH/PTHrP receptor (PTH1R) on chondrocytes in animals with osteoarthritis

<p>Abstract</p> <p>Background</p> <p>To evaluate the expression of the type 1 PTH/PTHrP receptor (PTH1R) on chondrocytes from hyaline cartilage over the course of osteoarthritis (OA).</p> <p>Methods</p> <p>In 12 NZW rabbits, the anterior cruciate ligament (ACL) was resected to create anterior instability of the knee. In 12 control rabbits, only a sham operation, without resection of the ACL, was performed. Four animals from each group were killed at 3, 6, and 12 weeks. After opening the knee joint, OA was macroscopically graded and hyaline cartilage of the load-bearing area was evaluated histologically according to the Mankin scale and by immunostaining for PTH1R.</p> <p>Results</p> <p>There was a positive linear correlation between the time after surgery and the macroscopic and histologic OA scores. The scores in the control group were constant over the time course. Immunostaining showed significantly less expression of PTH1R in the experimental compared to the control group after 6 (P < 0.05) and 12 weeks (P < 0.01). In the experimental group, a negative linear correlation between PTH1R expression and macroscopic and histologic grades was found.</p> <p>Conclusions</p> <p>The results show an in vivo decrease in the expression of PTH1R on chondrocytes over the time course of OA. Further studies are needed to evaluate whether new treatment approaches could evolve from this knowledge.</p

Protective Function of STAT3 in CVB3-Induced Myocarditis

The transcription factor signal transducer and activator of transcription 3 (STAT3) is an important mediator of the inflammatory process. We investigated the role of STAT3 in viral myocarditis and its possible role in the development to dilated cardiomyopathy. We used STAT3-deficent mice with a cardiomyocyte-restricted knockout and induced a viral myocarditis using Coxsackievirus B3 (CVB3) which induced a severe inflammation during the acute phase of the viral myocarditis. A complete virus clearance and an attenuated inflammation were examined in both groups WT and STAT3 KO mice 4 weeks after infection, but the cardiac function in STAT3 KO mice was significantly decreased in contrast to the infected WT mice. Interestingly, an increased expression of collagen I was detected in STAT3 KO mice compared to WT mice 4 weeks after CVB3 infection. Furthermore, the matrix degradation was reduced in STAT3 KO mice which might be an explanation for the observed matrix deposition. Consequently, we here demonstrate the protective function of STAT3 in CVB3-induced myocarditis. Since the cardiomyocyte-restricted knockout leads to an increased fibrosis, it can be assumed that STAT3 signalling in cardiomyocytes protects the heart against increased fibrosis through paracrine effects