2,180 research outputs found

    Landau-Khalatnikov-Fradkin Transformations and the Fermion Propagator in Quantum Electrodynamics

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    We study the gauge covariance of the massive fermion propagator in three as well as four dimensional Quantum Electrodynamics (QED). Starting from its value at the lowest order in perturbation theory, we evaluate a non-perturbative expression for it by means of its Landau-Khalatnikov-Fradkin (LKF) transformation. We compare the perturbative expansion of our findings with the known one loop results and observe perfect agreement upto a gauge parameter independent term, a difference permitted by the structure of the LKF transformations.Comment: 9 pages, no figures, uses revte

    The nonperturbative propagator and vertex in massless quenched QED_d

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    It is well known how multiplicative renormalizability of the fermion propagator, through its Schwinger-Dyson equation, imposes restrictions on the 3-point fermion-boson vertex in massless quenched quantum electrodynamics in 4-dimensions (QED4_4). Moreover, perturbation theory serves as an excellent guide for possible nonperturbative constructions of Green functions. We extend these ideas to arbitrary dimensions dd. The constraint of multiplicative renormalizability of the fermion propagator is generalized to a Landau-Khalatnikov-Fradkin transformation law in dd-dimensions and it naturally leads to a constraint on the fermion-boson vertex. We verify that this constraint is satisfied in perturbation theory at the one loop level in 3-dimensions. Based upon one loop perturbative calculation of the vertex, we find additional restrictions on its possible nonperturbative forms in arbitrary dimensions.Comment: 13 pages, no figures, latex (uses IOP style files

    Three point SUSY Ward identities without Ghosts

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    We utilise a non-local gauge transform which renders the entire action of SUSY QED invariant and respects the SUSY algebra modulo the gauge-fixing condition, to derive two- and three-point ghost-free SUSY Ward identities in SUSY QED. We use the cluster decomposition principle to find the Green's function Ward identities and then takes linear combinations of the latter to derive identities for the proper functions.Comment: 20 pages, no figures, typos correcte

    SMOKING IS A STRONG INDEPENDENT PREDICTOR FOR FUNCTIONAL SIGNIFICANCE OF INTERMEDIATE CORONARY LESIONS

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    Refiere un ejercicio para mejorar el estilo del periodista. Evoca la necesidad de escribir al menos con claridad corrección y naturalida

    Neonatal mortality in Sudan: analysis of the Sudan household survey, 2010

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    BACKGROUND: Sudan is classified as having insufficient progress in achieving the Millennium Development Goal (MDG-4), where the levels of child and infant mortality are among the highest in the region and the world. This study investigated factors associated with neonatal mortality in Sudan. Neonatal death is defined as death within the first 28 days of life. METHODS: This study analysed data from the Sudan Household Health Survey 2nd round, which was carried out in 2010. Total of 6,198 live-born infants delivered within the two years preceding the survey were included as the study population. Multivariate logistic regression was used to model neonatal mortality as a function of maternal health parameters, socioeconomic indicators and the sex of the child. RESULTS: There were 189 neonatal deaths out of 6,198 live births (3.0%). In the multiple logistic regression, the factors associated with neonatal mortality were advanced maternal age (≥ 40 years; OR = 2.4; 95% CI: 1.21, 4.78, p = 0.012), poor household wealth index (OR = 1.6; 95% CI: 1.18, 2.47, p = 0.005), male child (OR = 1.8; 95% CI: 1.31, 2.42, p < 0.001), delivery of baby by Caesarean section (OR = 1.6; 95% CI: 1.78, 2.42, p = 0.013) and delivery complications (OR = 1.4; 95% CI: 1.18, 2.15, p = 0.002). CONCLUSION: Public health interventions which target neonatal mortality reduction should adopt a risk-factor-based approach to detect pregnancy complications early and once identified, the health system should be strengthened so that these complications can be dealt with adequately

    Outbreak of Fatal Childhood Lead Poisoning Related to Artisanal Gold Mining in Northwestern Nigeria, 2010.

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    Background: In May 2010, a team of national and international organizations was assembled to investigate children's deaths due to lead poisoning in villages in northwestern Nigeria. Objectives: To determine the cause of the childhood lead poisoning outbreak, investigate risk factors for child mortality, and identify children aged <5 years in need of emergency chelation therapy for lead poisoning. Methods: We administered a cross-sectional, door-to-door questionnaire in two affected villages, collected blood from children aged 2-59 months, and soil samples from family compounds. Descriptive and bivariate analyses were performed with survey, blood-lead, and environmental data. Multivariate logistic regression techniques were used to determine risk factors for childhood mortality. Results: We surveyed 119 family compounds. One hundred eighteen of 463 (25%) children aged <5 years had died in the last year. We tested 59% (204/345) of children, aged <5 years, and all were lead poisoned (≥10 µg/dL); 97% (198/204) of children had blood-lead levels ≥45 µg/dL, the threshold for initiating chelation therapy. Gold ore was processed inside two-thirds of the family compounds surveyed. In multivariate modeling significant risk factors for death in the previous year from suspected lead poisoning included: the child's age, the mother performing ore-processing activities, community well as primary water source, and the soil-lead concentration in the compound. Conclusion: The high levels of environmental contamination, percentage of children aged <5 years with elevated blood-lead levels (97%, >45 µg/dL), and incidence of convulsions among children prior to death (82%) suggest that most of the recent childhood deaths in the two surveyed villages were caused by acute lead poisoning from gold ore-processing activities. Control measures included environmental remediation, chelation therapy, public health education, and control of mining activities

    The Mare as a Model for Luteinized Unruptured Follicle Syndrome: Intrafollicular Endocrine Milieu.

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    Luteinized unruptured follicle (LUF) syndrome is a recurrent anovulatory dysfunction that affects up to 23% of women with normal menstrual cycles and up to 73% with endometriosis. Mechanisms underlying the development of LUF syndrome in mares were studied to provide a potential model for human anovulation. The effect of extended increase in circulating LH achieved by administration of recombinant equine LH (reLH) or a short surge of LH and decrease in progesterone induced by prostaglandin F2α (PGF2α) on LUF formation (Experiment 1), identification of an optimal dose of COX-2 inhibitor (flunixin meglumine, FM; to block the effect of prostaglandins) for inducing LUFs (Experiment 2), and evaluation of intrafollicular endocrine milieu in LUFs (Experiment 3) were investigated. In Experiment 1, mares were treated with reLH from Day 7 to Day 15 (Day 0=ovulation), PGF2α on Day 7, or in combination. In Experiment 2, FM at doses of 2.0 or 3.0 mg/kg every 12 h and human chorionic gonadotropin (hCG) (1500 IU) were administered after a follicle ≥32 mm was detected. In Experiment 3, FM at a dose of 2.0 mg/kg every 12 h plus hCG was used to induce LUFs and investigate the intrafollicular endocrine milieu. No LUFs were induced by reLH or PGF2α treatment; however, LUFs were induced in 100% of mares using FM. Intrafollicular PGF2α metabolite, PGF2α, and PGE2 were lower and the ratio of PGE2:PGF2α was higher in the induced LUF group. Higher levels of intrafollicular E2 and total primary sex steroids were observed in the induced LUF group along with a tendency for higher levels of GH, cortisol, and T; however, LH, PRL, VEGF-A, and NO did not differ between groups. In conclusion, this study reveals part of the intrafollicular endocrine milieu and the association of prostaglandins in LUF formation, and indicates that the mare might be an appropriate model for studying the poorly understood LUF syndrome
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