Room temperature coherent control of coupled single spins in solid

Coherent coupling between single quantum objects is at the heart of modern quantum physics. When coupling is strong enough to prevail over decoherence, it can be used for the engineering of correlated quantum states. Especially for solid-state systems, control of quantum correlations has attracted widespread attention because of applications in quantum computing. Such coherent coupling has been demonstrated in a variety of systems at low temperature1, 2. Of all quantum systems, spins are potentially the most important, because they offer very long phase memories, sometimes even at room temperature. Although precise control of spins is well established in conventional magnetic resonance3, 4, existing techniques usually do not allow the readout of single spins because of limited sensitivity. In this paper, we explore dipolar magnetic coupling between two single defects in diamond (nitrogen-vacancy and nitrogen) using optical readout of the single nitrogen-vacancy spin states. Long phase memory combined with a defect separation of a few lattice spacings allow us to explore the strong magnetic coupling regime. As the two-defect system was well-isolated from other defects, the long phase memory times of the single spins was not diminished, despite the fact that dipolar interactions are usually seen as undesirable sources of decoherence. A coherent superposition of spin pair quantum states was achieved. The dipolar coupling was used to transfer spin polarisation from a nitrogen-vacancy centre spin to a nitrogen spin, with optical pumping of a nitrogen-vacancy centre leading to efficient initialisation. At the level anticrossing efficient nuclear spin polarisation was achieved. Our results demonstrate an important step towards controlled spin coupling and multi-particle entanglement in the solid state

What do minerals in the feces of Bearded Vultures reveal about their dietary habits?

The diet of Bearded Vultures Gypaetus barbatus consists mainly of bones, which are completely digested in the gastrointestinal tract, unwanted bone minerals being discarded via the feces. Chemical analyses of feces therefore provide a noninvasive technique for studying the diet of this species. We analysed the inorganic and organic remains in feces collected from Bearded Vulture nests in the Spanish Pyrenees and discussed these results with the diet of individuals determined by video camera observations. Of the food items delivered to the nest, taxonomically 65% were bone fragments of Ovis/Capra spp. (range 56–75%) and anatomically 76% (74–81%) bones from the extremities, indicating a selective preference. At least 15% of the diet was meat based, mainly originating from small prey (e.g. small carnivores, birds). The fecal analyses show that calcium and phosphorus are the most abundant mineral constituents, accounting for 41.3–44.4% of the mineral part of the feces. Among the minor elements identified, the variation in the concentrations of iron, silicon and zinc suggest differences in food selection between territories, although this could be related to varying amounts of accidentally ingested soil particles present in the food. We found variation in the content of uric acid in the feces, ranging between 0.5 and 4.6%. Higher values of uric acid might be due to a more meat or marrow bone-based diet. However, no relationship was found between the amount of calcium and uric acid levels, suggesting that the metabolites of meat digestion (uric acid) and those of bone digestion (calcium) are not negatively correlated as expected. In conclusion, our chemical analyses of feces collected from the nests of Bearded Vultures confirm that their diet consists mainly of bone remains and that these bones are digested completely. However, the direct observations of the prey items delivered to the nest produced more detailed information than the chemical analyses.This project was partially funded by Ministerio de Ciencia, Innovación y Universidades (project RTI2018-099609-B-C22).Peer reviewe

Replacement of l-Amino Acids by d-Amino Acids in the Antimicrobial Peptide Ranalexin and Its Consequences for Antimicrobial Activity and Biodistribution

Infections caused by multidrug-resistant bacteria are a global emerging problem. New antibiotics that rely on innovative modes of action are urgently needed. Ranalexin is a potent antimicrobial peptide (AMP) produced in the skin of the American bullfrog Rana catesbeiana. Despite strong antimicrobial activity against Gram-positive bacteria, ranalexin shows disadvantages such as poor pharmacokinetics. To tackle these problems, a ranalexin derivative consisting exclusively of d-amino acids (named danalexin) was synthesized and compared to the original ranalexin for its antimicrobial potential and its biodistribution properties in a rat model. Danalexin showed improved biodistribution with an extended retention in the organisms of Wistar rats when compared to ranalexin. While ranalexin is rapidly cleared from the body, danalexin is retained primarily in the kidneys. Remarkably, both peptides showed strong antimicrobial activity against Gram-positive bacteria and Gram-negative bacteria of the genus Acinetobacter with minimum inhibitory concentrations (MICs) between 4 and 16 mg/L (1.9–7.6 µM). Moreover, both peptides showed lower antimicrobial activities with MICs ≥32 mg/L (≥15.2 µM) against further Gram-negative bacteria. The preservation of antimicrobial activity proves that the configuration of the amino acids does not affect the anticipated mechanism of action, namely pore formation

Whole blood transcriptomics in cardiac surgery identifies a gene regulatory network connecting ischemia reperfusion with systemic inflammation.

BACKGROUND: Cardiac surgery with cardiopulmonary bypass (CS/CPB) is associated with increased risk for postoperative complications causing substantial morbidity and mortality. To identify the molecular mechanisms underlying CS/CPB-induced pathophysiology we employed an integrative systems biology approach using the whole blood transcriptome as the sentinel organ. METHODOLOGY/PRINCIPAL FINDINGS: Total RNA was isolated and globin mRNA depleted from whole blood samples prospectively collected from 10 patients at time points prior (0), 2 and 24 hours following CS/CPB. Genome-wide transcriptional analysis revealed differential expression of 610 genes after CS/CPB (p<0.01). Among the 375 CS/CPB-upregulated genes, we found a gene-regulatory network consisting of 50 genes, reminiscent of activation of a coordinated genetic program triggered by CS/CPB. Intriguingly, the highly connected hub nodes of the identified network included key sensors of ischemia-reperfusion (HIF-1alpha and C/EBPbeta). Activation of this network initiated a concerted inflammatory response via upregulation of TLR-4/5, IL1R2/IL1RAP, IL6, IL18/IL18R1/IL18RAP, MMP9, HGF/HGFR, CalgranulinA/B, and coagulation factors F5/F12 among others. Differential regulation of 13 candidate genes including novel, not hitherto CS/CBP-associated genes, such as PTX3, PGK1 and Resistin, was confirmed using real-time quantitative RT-PCR. In support of the mRNA data, differential expression of MMP9, MIP1alpha and MIP1beta plasma proteins was further confirmed in 34 additional patients. CONCLUSIONS: Analysis of blood transcriptome uncovered critical signaling pathways governing the CS/CPB-induced pathophysiology. The molecular signaling underlying ischemia reperfusion and inflammatory response is highly intertwined and includes pro-inflammatory as well as cardioprotective elements. The herein identified candidate genes and pathways may provide promising prognostic biomarker and therapeutic targets

Modifying the Mitochondrial Genome

Human mitochondria produce ATP and metabolites to support development and maintain cellular homeostasis. Mitochondria harbor multiple copies of a maternally-inherited, non-nuclear genome (mtDNA) that encodes for 13 subunit proteins of the respiratory chain. Mutations in mtDNA occur mainly in the 24 non-coding genes, with specific mutations implicated in early death, neuromuscular and neurodegenerative diseases, cancer, and diabetes. A significant barrier to new insights in mitochondrial biology and clinical applications for mtDNA disorders is our general inability to manipulate the mtDNA sequence. Microinjection, cytoplasmic fusion, nucleic acid import strategies, targeted endonucleases, and newer approaches that include the transfer of genomic DNA, somatic cell reprogramming, and a photothermal nanoblade, attempt to change the mtDNA sequence in target cells with varying efficiencies and limitations. Here, we discuss the current state of manipulating mammalian mtDNA and provide an outlook for mitochondrial reverse genetics, which could further enable mitochondrial research and therapies for mtDNA diseases