253 research outputs found
Using theorem provers to increase the precision of dependence analysis for information flow control
Information flow control (IFC) is a category of techniques for enforcing information flow properties. In this paper we present the Combined Approach, a novel IFC technique that combines a scalable system-dependence-graph-based (SDG-based) approach with a precise logic-based approach based on a theorem prover. The Combined Approach has an increased precision compared with the SDG-based approach on its own, without sacrificing its scalability. For every potential illegal information flow reported by the SDG-based approach, the Combined Approach automatically generates proof obligations that, if valid, prove that there is no program path for which the reported information flow can happen. These proof obligations are then relayed to the logic-based approach. We also show how the SDG-based approach can provide additional information to the theorem prover that helps decrease the verification effort. Moreover, we present a prototypical implementation of the Combined Approach that uses the tools JOANA and KeY as the SDG-based and logic-based approach respectively
Quantum interface of an electron and a nuclear ensemble.
Coherent excitation of an ensemble of quantum objects underpins quantum many-body phenomena and offers the opportunity to realize a memory that stores quantum information. Thus far, a deterministic and coherent interface between a spin qubit and such an ensemble has remained elusive. In this study, we first used an electron to cool the mesoscopic nuclear spin ensemble of a semiconductor quantum dot to the nuclear sideband-resolved regime. We then implemented an all-optical approach to access individual quantized electronic-nuclear spin transitions. Lastly, we performed coherent optical rotations of a single collective nuclear spin excitation-a spin wave. These results constitute the building blocks of a dedicated local memory per quantum-dot spin qubit and promise a solid-state platform for quantum-state engineering of isolated many-body systems
The inverse-trans-influence in tetravalent lanthanide and actinide bis(carbene) complexes
Across the periodic table the trans-influence operates, whereby tightly bonded ligands selectively lengthen mutually trans metal–ligand bonds. Conversely, in high oxidation state actinide complexes the inverse-trans-influence operates, where normally cis strongly donating ligands instead reside trans and actually reinforce each other. However, because the inversetrans-influence is restricted to high-valent actinyls and a few uranium(V/VI) complexes, it has had limited scope in an area with few unifying rules. Here we report tetravalent cerium, uranium and thorium bis(carbene) complexes with trans C¼M¼C cores where experimental and theoretical data suggest the presence of an inverse-trans-influence. Studies of hypothetical praseodymium(IV) and terbium(IV) analogues suggest the inverse-trans-influence may extend to these ions but it also diminishes significantly as the 4f orbitals are populated. This work suggests that the inverse-trans-influence may occur beyond high oxidation state 5f metals and hence could encompass mid-range oxidation state actinides and lanthanides. Thus, the inverse-trans-influence might be a more general f-block principle
Molecular and electronic structure of terminal and alkali metal-capped uranium(V) nitride complexes
Determining the electronic structure of actinide complexes is intrinsically challenging because inter-electronic repulsion, crystal field, and spin–orbit coupling effects can be of similar magnitude. Moreover, such efforts have been hampered by the lack of structurally analogous families of complexes to study. Here we report an improved method to U≡N triple bonds, and assemble a family of uranium(V) nitrides. Along with an isoelectronic oxo, we quantify the electronic structure of this 5f1 family by magnetometry, optical and electron paramagnetic resonance (EPR) spectroscopies and modelling. Thus, we define the relative importance of the spin–orbit and crystal field interactions, and explain the experimentally observed different ground states. We find optical absorption linewidths give a potential tool to identify spin–orbit coupled states, and show measurement of UV···UV super-exchange coupling in dimers by EPR. We show that observed slow magnetic relaxation occurs via two-phonon processes, with no obvious correlation to the crystal field
Abnormal spatial diffusion of Ca2+ in F508del-CFTR airway epithelial cells
<p>Abstract</p> <p>Background</p> <p>In airway epithelial cells, calcium mobilization can be elicited by selective autocrine and/or paracrine activation of apical or basolateral membrane heterotrimeric G protein-coupled receptors linked to phospholipase C (PLC) stimulation, which generates inositol 1,4,5-trisphosphate (IP<sub>3</sub>) and 1,2-diacylglycerol (DAG) and induces Ca<sup>2+ </sup>release from endoplasmic reticulum (ER) stores.</p> <p>Methods</p> <p>In the present study, we monitored the cytosolic Ca<sup>2+ </sup>transients using the UV light photolysis technique to uncage caged Ca<sup>2+ </sup>or caged IP<sub>3 </sub>into the cytosol of loaded airway epithelial cells of cystic fibrosis (CF) and non-CF origin. We compared in these cells the types of Ca<sup>2+ </sup>receptors present in the ER, and measured their Ca<sup>2+ </sup>dependent activity before and after correction of F508del-CFTR abnormal trafficking either by low temperature or by the pharmacological corrector miglustat (N-butyldeoxynojirimycin).</p> <p>Results</p> <p>We showed reduction of the inositol 1,4,5-trisphosphate receptors (IP<sub>3</sub>R) dependent-Ca<sup>2+ </sup>response following both correcting treatments compared to uncorrected cells in such a way that Ca<sup>2+ </sup>responses (CF+treatment <it>vs </it>wild-type cells) were normalized. This normalization of the Ca<sup>2+ </sup>rate does not affect the activity of Ca<sup>2+</sup>-dependent chloride channel in miglustat-treated CF cells. Using two inhibitors of IP<sub>3</sub>R1, we observed a decrease of the implication of IP<sub>3</sub>R1 in the Ca<sup>2+ </sup>response in CF corrected cells. We observed a similar Ca<sup>2+ </sup>mobilization between CF-KM4 cells and CFTR-cDNA transfected CF cells (CF-KM4-reverted). When we restored the F508del-CFTR trafficking in CFTR-reverted cells, the specific IP<sub>3</sub>R activity was also reduced to a similar level as in non CF cells. At the structural level, the ER morphology of CF cells was highly condensed around the nucleus while in non CF cells or corrected CF cells the ER was extended at the totality of cell.</p> <p>Conclusion</p> <p>These results suggest reversal of the IP<sub>3</sub>R dysfunction in F508del-CFTR epithelial cells by correction of the abnormal trafficking of F508del-CFTR in cystic fibrosis cells. Moreover, using CFTR cDNA-transfected CF cells, we demonstrated that abnormal increase of IP<sub>3</sub>R Ca<sup>2+ </sup>release in CF human epithelial cells could be the consequence of F508del-CFTR retention in ER compartment.</p
The Potential for pathogenicity was present in the ancestor of the Ascomycete subphylum Pezizomycotina
<p>Abstract</p> <p>Background</p> <p>Previous studies in Ascomycetes have shown that the function of gene families of which the size is considerably larger in extant pathogens than in non-pathogens could be related to pathogenicity traits. However, by only comparing gene inventories in extant species, no insights can be gained into the evolutionary process that gave rise to these larger family sizes in pathogens. Moreover, most studies which consider gene families in extant species only tend to explain observed differences in gene family sizes by gains rather than by losses, hereby largely underestimating the impact of gene loss during genome evolution.</p> <p>Results</p> <p>In our study we used a selection of recently published genomes of Ascomycetes to analyze how gene family gains, duplications and losses have affected the origin of pathogenic traits. By analyzing the evolutionary history of gene families we found that most gene families with an enlarged size in pathogens were present in an ancestor common to both pathogens and non-pathogens. The majority of these families were selectively maintained in pathogenic lineages, but disappeared in non-pathogens. Non-pathogen-specific losses largely outnumbered pathogen-specific losses.</p> <p>Conclusions</p> <p>We conclude that most of the proteins for pathogenicity were already present in the ancestor of the Ascomycete lineages we used in our study. Species that did not develop pathogenicity seemed to have reduced their genetic complexity compared to their ancestors. We further show that expansion of gained or already existing families in a species-specific way is important to fine-tune the specificities of the pathogenic host-fungus interaction.</p
A Community Study of Factors Related to Poorly Controlled Asthma among Brazilian Urban Children
BACKGROUND: Asthma constitutes a serious public health problem in many regions of the world, including the city of Salvador, State of Bahia-Brazil. The purpose of this study was to analyse the factors associated with poor asthma control. METHODOLOGY/PRINCIPAL FINDINGS: Two definitions were used for asthma: 1) wheezing in the last 12 months; 2) wheezing in the last 12 months plus other asthma symptoms or asthma diagnosis ever. The definition of poorly controlled asthma was: at least one reported hospitalisation due to asthma and/or high frequency of symptoms, in the last year. Children with poorly controlled asthma (N = 187/374) were compared with wheezing children with controlled asthma regarding age, gender, atopy, parental asthma, rhinitis, eczema, exposure to second hand tobacco smoke, presence of moulds, pets and pests in the house, helminth infections and body mass index. Crude and logistic regression adjusted odds ratios were used as measures of association. There was a higher proportion of poorly controlled asthma among children with eczema (OR = 1.55; 95% CI 1.02; 2.37). The strength of the association was greater among children with eczema and rhinitis (42.6%, 53.4% and 57.7%, respectively, in children who had no rhinitis nor eczema, had only one of those, and had both (p = 0.02 for trend test). The presence of mould in the houses was inversely associated with poorly controlled asthma (OR = 0.54; 95% CI 0.34; 0.87). CONCLUSIONS/SIGNIFICANCE: Our results indicate an association between eczema and poor asthma control in this environment, but emphasize the role of various other individual and environmental factors as determinants of poor control
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