ABSTRACT
Dielectric properties and impedance spectroscopic studies of single phase Zn1- xCoxO (0 ≤ x ≤ 0.05) ceramics, synthesized by a pressure-less solid state reaction method, have been carried out to investigate the origin of colossal dielectric permittivity (CP), ε' â¼ 105, in a wide frequency (2 × 101-2 × 106 Hz) range. These results show that a defect density within the grain is present in the materials due to the use of pressure-less sintering at high temperature for a long duration of time. The colossal dielectric response is essentially due to this electronic inhomogeneous conduction mechanism within the material due to the production of absorption current in the thin grain boundary region which accumulates charge at the interface and induces Maxwell-Wagner interfacial polarization. Moreover, this defect structure further increases with the addition of Co ions and enhances the CP property. An effective way to control the colossal dielectric properties is to control the defect density within a grain by using a proper sintering method.
ABSTRACT
OBJECTIVE: To examine the relationship between birth weight, gestational age, small for gestational age (SGA), and 3 of the most common autism spectrum disorder (ASD) subtypes. STUDY DESIGN: In this population-based case-control study conducted in Finland, 4713 cases born between 1987 and 2005 with International Classification of Diseases-diagnoses of childhood autism, Asperger syndrome, or pervasive developmental disorder (PDD), were ascertained from the Finnish Hospital Discharge Register. Four controls, individually matched on sex, date of birth, and place of birth, were selected from the Finnish Medical Birth Register for each case. Conditional logistic regression models were used to assess whether birth weight and gestational age information predicted ASD after controlling for maternal age, parity, smoking during pregnancy, and psychiatric history, as well as for infant's major congenital anomalies. RESULTS: Very low (<1500 g) and moderately low (<2500 g) birth weight, very low gestational age (less than 32 weeks), and SGA increased risk of childhood autism (adjusted OR 3.05, 95% CI 1.4-6.5; 1.57, 1.1-2.3; 2.51, 1.3-5.0; and 1.72, 1.1-2.6, respectively). Very low and moderately low birth weight, very low gestational age, and SGA were also associated with increase in PDD risk (OR 3.44, 95% CI 1.9-6.3; 1.81, 1.4-2.4; 2.46, 1.4-2.3; and 2.24, 1.7-3.0, respectively). No associations were found between the perinatal characteristics and Asperger syndrome. The increased risks persisted after controlling for selected potential confounders. CONCLUSIONS: The finding that low birth weight, prematurity, and SGA were related to childhood autism and PDD but not to Asperger syndrome suggests that prenatal factors related to these exposures may differ for these ASD subtypes, which may have preventive implications.
Subject(s)
Child Development Disorders, Pervasive/diagnosis , Infant, Premature, Diseases/diagnosis , Birth Weight , Case-Control Studies , Child , Child Development Disorders, Pervasive/etiology , Child, Preschool , Developmental Disabilities/diagnosis , Female , Finland , Follow-Up Studies , Humans , Infant , Infant, Newborn , Infant, Small for Gestational Age , Male , Registries , Regression Analysis , Risk , Risk FactorsABSTRACT
We report observation of the electroweak production of single top quarks in pp[over ] collisions at sqrt[s]=1.96 TeV based on 2.3 fb(-1) of data collected by the D0 detector at the Fermilab Tevatron Collider. Using events containing an isolated electron or muon and missing transverse energy, together with jets originating from the fragmentation of b quarks, we measure a cross section of sigma(pp[over ]--> tb + X, tqb + X) = 3.94 + or - 0.88 pb. The probability to measure a cross section at this value or higher in the absence of signal is 2.5 x 10(-7), corresponding to a 5.0 standard deviation significance for the observation.
ABSTRACT
We present a search for a narrow resonance in the inclusive diphoton final state using approximately 2.7 fb(-1) of data collected with the D0 detector at the Fermilab Tevatron pp Collider. We observe good agreement between the data and the background prediction, and set the first 95% C.L. upper limits on the production cross section times the branching ratio for decay into a pair of photons for resonance masses between 100 and 150 GeV. This search is also interpreted in the context of several models of electroweak symmetry breaking with a Higgs boson decaying into two photons.
ABSTRACT
We present a search for direct CP violation in B(+/-)-->J/psiK(+/-)(pi(+/-)) decays. The event sample is selected from 2.8 fb(-1) of pp collisions recorded by D0 experiment in run II of the Fermilab Tevatron Collider. The charge asymmetry A_(CP)(B(+)-->J/psiK(+))= + 0.0075 +/- 0.0061(stat)+/-0.0030(syst) is obtained using a sample of approximately 40, 000 B(+/-)-->J/psiK(+/-) decays. The achieved precision is of the same level as the expected deviation predicted by some extensions of the standard model. We also measured the charge asymmetry A(CP)(B(+)-->J/psipi(+))=-0.09+/-0.08(stat)+/-0.03(syst).
ABSTRACT
We search for the production of a heavy W' gauge boson that decays to third generation quarks in 0.9 fb-1 of pp collisions at square root(s)=1.96 TeV, collected with the D0 detector at the Fermilab Tevatron collider. We find no significant excess in the final-state invariant mass distribution and set upper limits on the production cross section times branching fraction. For a left-handed W' boson with SM couplings, we set a lower mass limit of 731 GeV. For right-handed W' bosons, we set lower mass limits of 739 GeV if the W' boson decays to both leptons and quarks and 768 GeV if the W' boson decays only to quarks. We also set limits on the coupling of the W' boson to fermions as a function of its mass.
ABSTRACT
We present a search for associated Higgs boson production in the process pp-->WH-->WWW*-->l;+/-nul'+/-nu'+X in final states containing two like-sign isolated electrons or muons (e+/-e;+/-, e+/-micro+/-, or micro+/-micro+/-). The search is based on D0 run II data samples corresponding to integrated luminosities of 360-380 pb-1. No excess is observed over the predicted standard model background. We set 95% C.L. upper limits on sigma(pp-->WH)xBr(H-->WW*) between 3.2 and 2.8 pb for Higgs boson masses from 115 to 175 GeV.
ABSTRACT
Retinitis pigmentosa (RP) is a heterogeneous genetic disorder with autosomal dominant, autosomal recessive, and X-linked forms. We previously mapped an additional arRP locus to chromosome 6p21 (RP14) in a single extended kinship from the Dominican Republic. Aided by a second linked RP pedigree from the same region of the Dominican Republic, we have refined the disease locus to a 2-cM region that is homozygous-by-descent in both pedigrees. A complete YAC, and a partial BAC, contig of the RP14 locus was constructed between the markers D6S1560 and D6S291, encompassing approximately 2.1 Mb. The contig contains 12 YACs and 31 BACs and is characterized by 45 markers including 8 microsatellite markers, 6 gene-derived sequences/ESTs obtained from the databases, and 28 new STSs and 4 new ESTs obtained by BLAST search using DNA sequence from the ends of the BAC and YAC inserts. With a STS density of approximately 1 every 20 kilobases, this contig significantly enhances available maps of the region.
Subject(s)
Chromosome Mapping , Chromosomes, Human, Pair 6/genetics , Genes, Recessive/genetics , Homozygote , Restriction Mapping , Retinitis Pigmentosa/genetics , Chromosomes, Artificial, Yeast/genetics , Chromosomes, Artificial, Yeast/metabolism , Chromosomes, Bacterial/genetics , Cloning, Molecular , Dominican Republic , Female , Genetic Markers , Humans , Male , PedigreeABSTRACT
The RP14 autosomal recessive Retinitis pigmentosa (arRP) locus has been mapped to a 2cM region of chromosome 6p21.3. TULP1 (the gene encoding tubby-like protein 1) is a candidate target for the disease mutation because it maps to the RP14 minimum genetic region and because a mutation in the highly homologous mouse tub gene leads to obesity, deafness and early progressive retinal degeneration. Here we report a splice-site mutation (IVS14+1, G-->A) that is homozygous in all affected individuals (N=33) and heterozygous in all obligate carriers (N=50) from two RP14-linked kindreds. The mutation was not observed in 210 unrelated controls. The data indicate that impairment of TULP1 protein function is a rare cause of arRP and that the normal protein plays an essential role in the physiology of the retina.