Quantum non-demolition measurements of single donor spins in semiconductors

We propose a technique for measuring the state of a single donor electron spin using a field-effect transistor induced two-dimensional electron gas and electrically detected magnetic resonance techniques. The scheme is facilitated by hyperfine coupling to the donor nucleus. We analyze the potential sensitivity and outline experimental requirements. Our measurement provides a single-shot, projective, and quantum non-demolition measurement of an electron-encoded qubit state.Comment: 8+ pages. 4 figures. Published versio

Infection Regulates Pro-Resolving Mediators that Lower Antibiotic Requirements

Underlying mechanisms for how bacterial infections contribute to active resolution of acute inflammation are unknown. Here, we performed exudate leukocyte trafficking and mediator-metabololipidomics of murine peritoneal Escherichia coli (E. coli) infections with temporal identification of pro-inflammatory (prostaglandins and leukotrienes) and specialized pro-resolving mediators (SPM). In self-resolving E. coli exudates ($10^5$ CFU), the dominant SPM identified were resolvin (Rv) D5 and protectin D1 (PD1), which at 12 h were significantly greater than levels in exudates from higher titer E. coli ($10^7$ CFU) challenged mice. Germ-free mice displayed endogenous RvD1 and PD1 levels higher than in conventional mice. RvD1 and RvD5 (ng/mouse) each reduced bacterial titers in blood and exudates, E. coli-induced hypothermia and increased survival, demonstrating the first actions of RvD5. With human polymorphonuclear neutrophils (PMN) and macrophages, RvD1, RvD5, and PD1 each directly enhanced phagocytosis of E. coli, and RvD5 counter-regulated a panel of pro-inflammatory genes, including NF-κB and TNF-α. RvD5 activated the RvD1 receptor, GPR32, to enhance phagocytosis. With self-limited E. coli infections, RvD1 and the antibiotic ciprofloxacin accelerated resolution, each shortening resolution intervals (Ri). Host-directed RvD1 actions enhanced ciprofloxacin’s therapeutic actions. In $10^7$ CFU E. coli infections, SPM (RvD1, RvD5, PD1) together with ciprofloxacin also heightened host antimicrobial responses. In skin infections, SPM enhanced vancomycin clearance of Staphylococcus aureus. These results demonstrate that specific SPM are temporally and differentially regulated during infections and that they are anti-phlogistic, enhance containment and lower antibiotic requirements for bacterial clearance

Kinetic Energy Release Distributions for C⁺₂ Emission from Multiply Charged C₆₀ and C₇₀ Fullerenes

We present asystematic study of experimental kinetic energy release distributions for the asymmetric fission processes Cq+60 C(iq-1\u3c)+70+ C+2 and C q+70 C(q-1)+60+ C+ 2 for mother ions incharge states q 4-8 produced incollisions with slow highly charged ions. Somewhat to our surprise, we find that the KERD for asymmetric fission from Cq+60 are considerably wider and have larger most likely values than the Cq+70 distributions inthe corresponding charge states when q \u3e 4

Lipoxin A4 stable analogs reduce allergic airway responses via mechanisms distinct from CysLT1 receptor antagonism

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/154665/1/fsb2fj078653com.pd

Electronic structure of superposition states in flux qubits

Flux qubits, small superconducting loops interrupted by Josephson junctions, are successful realizations of quantum coherence for macroscopic variables. Superconductivity in these loops is carried by $\sim 10^6$ -- $10^{10}$ electrons, which has been interpreted as suggesting that coherent superpositions of such current states are macroscopic superpositions analogous to Schr\"odinger's cat. We provide a full microscopic analysis of such qubits, from which the macroscopic quantum description can be derived. This reveals that the number of microscopic constituents participating in superposition states for experimentally accessible flux qubits is surprisingly but not trivially small. The combination of this relatively small size with large differences between macroscopic observables in the two branches is seen to result from the Fermi statistics of the electrons and the large disparity between the values of superfluid and Fermi velocity in these systems.Comment: Minor cosmetic changes. Published version

CCDC26, CDKN2BAS, RTEL1 and TERT Polymorphisms in pediatric brain tumor susceptibility

The role of genetic polymorphisms in pediatric brain tumor (PBT) etiology is poorly understood. In this study, we tested the hypothesis that single nucleotide polymorphisms identified by genome-wide association studies on adult glioma are also associated with PBT ris

CCDC26, CDKN2BAS, RTEL1 and TERT Polymorphisms in pediatric brain tumor susceptibility

The role of genetic polymorphisms in pediatric brain tumor (PBT) etiology is poorly understood. In this study, we tested the hypothesis that single nucleotide polymorphisms identified by genome-wide association studies on adult glioma are also associated with PBT ris

A multinational case-control study on childhood brain tumours, anthropogenic factors, birth characteristics and prenatal exposures: A validation of interview data.

Little is known about the aetiology of childhood brain tumours. We investigated anthropometric factors (birth weight, length, maternal age), birth characteristics (e.g. vacuum extraction, preterm delivery, birth order) and exposures during pregnancy (e.g. maternal: smoking, working, dietary supplement intake) in relation to risk of brain tumour diagnosis among 7-19 year olds. The multinational case-control study in Denmark, Sweden, Norway and Switzerland (CEFALO) included interviews with 352 (participation rate=83.2%) eligible cases and 646 (71.1%) population-based controls. Interview data were complemented with data from birth registries and validated by assessing agreement (Cohen's Kappa). We used conditional logistic regression models matched on age, sex and geographical region (adjusted for maternal age and parental education) to explore associations between birth factors and childhood brain tumour risk. Agreement between interview and birth registry data ranged from moderate (Kappa=0.54; worked during pregnancy) to almost perfect (Kappa=0.98; birth weight). Neither anthropogenic factors nor birth characteristics were associated with childhood brain tumour risk. Maternal vitamin intake during pregnancy was indicative of a protective effect (OR 0.75, 95%-CI: 0.56-1.01). No association was seen for maternal smoking during pregnancy or working during pregnancy. We found little evidence that the considered birth factors were related to brain tumour risk among children and adolescents

Mobile Phone Use and Brain Tumors in Children and Adolescents: A Multicenter Case-Control Study

Background It has been hypothesized that children and adolescents might be more vulnerable to possible health effects from mobile phone exposure than adults. We investigated whether mobile phone use is associated with brain tumor risk among children and adolescents. Methods CEFALO is a multicenter case-control study conducted in Denmark, Sweden, Norway, and Switzerland that includes all children and adolescents aged 7-19 years who were diagnosed with a brain tumor between 2004 and 2008. We conducted interviews, in person, with 352 case patients (participation rate: 83%) and 646 control subjects (participation rate: 71%) and their parents. Control subjects were randomly selected from population registries and matched by age, sex, and geographical region. We asked about mobile phone use and included mobile phone operator records when available. Odds ratios (ORs) for brain tumor risk and 95% confidence intervals (CIs) were calculated using conditional logistic regression models. Results Regular users of mobile phones were not statistically significantly more likely to have been diagnosed with brain tumors compared with nonusers (OR = 1.36; 95% CI = 0.92 to 2.02). Children who started to use mobile phones at least 5 years ago were not at increased risk compared with those who had never regularly used mobile phones (OR = 1.26, 95% CI = 0.70 to 2.28). In a subset of study participants for whom operator recorded data were available, brain tumor risk was related to the time elapsed since the mobile phone subscription was started but not to amount of use. No increased risk of brain tumors was observed for brain areas receiving the highest amount of exposure. Conclusion The absence of an exposure-response relationship either in terms of the amount of mobile phone use or by localization of the brain tumor argues against a causal associatio