How To Fix Non-Perturbatively A Parameter Dependent Covariant Gauge On The Lattice

We describe how to overcome some problems that usually prevent from obtaining an efficient algorithm to fix a generic covariant gauge on the lattice. This gauge is the lattice equivalent of the generic gauge usually adopted in perturbative calculations. It depends on a parameter whose value can be varied in order to check the gauge dependence of measured matrix elements.Comment: 3 pages, 2 eps figures, LATTICE 9

On the Definition of Gauge Field Operators in Lattice Gauge-Fixed Theories

We address the problem of defining the gauge four-potential on the lattice, in terms of the natural link variables. Different regularized definitions are shown, through non perturbative numerical computation, to converge towards the same continuum renormalized limit.Comment: 8 pages, LaTeX2e/LaTeX209, 3 eps figure

Glue Ball Masses and the Chameleon Gauge

We introduce a new numerical technique to compute mass spectra, based on difference method and on a new gauge fixing procedure. We show that the method is very effective by test runs on a $SU(2)$ lattice gauge theory.Comment: latex format, 10 pages, 4 figures added in uufiles forma

Quark and Gluon Propagators in Covariant Gauges

We present data for the gluon and quark propagators computed in the standard lattice Landau's gauge and for three values of the covariant gauge-fixing parameter lambda=0,8,16. Our results are obtained using the SU(3) Wilson action in the quenched approximation at beta=6.0 and volume=16^3x32.Comment: Lattice2001(theorydevelop

Family study of epilepsy in first degree relatives: Data from the Italian Episcreen study

Objective: To evaluate the family history of epilepsy in first degree relatives of probands with epilepsy. Methods: A sample of 10787 patients with epilepsy with complete information about first degree relatives (parents, siblings and offspring) was selected from the database of the Episcreen Project, the largest Italian observational study on epilepsy. Family history was assessed by: (1) prevalence estimates of epilepsy among proband's relatives, (2) modified cumulative risks (MCR), adjusted using proband's age as censoring time in life tables, (3) standardised morbidity ratios (SMR), using a sub-group of symptomatic epilepsies as control group. Results: Patients (9.1%) had a family history of epilepsy. The overall prevalence of epilepsy among first degree relatives was 2.6%. Idiopathic generalised epilepsies had the highest prevalence (5.3%). Cryptogenetic epilepsies had a lower prevalence (2.1%) than idiopathic epilepsies, but higher then symptomatic epilepsies (1.5%), both in generalised and focal forms (3.8% vs. 2.0% and 1.8% vs. 1.3%). A similar tendency was detected using MCR and SMR, with the higher values of risks/ratios for idiopathic and generalised epilepsies. Probands with idiopathic generalised epilepsies were highly concordant with respect to their relatives' type of epilepsy. Considering other strata factors, risks were higher in proband's epilepsies with an onset less then 14 years of age, while sex played no definite role in differentiating the family history. Conclusions: The Episcreen model permits a variety of stratification factors to measure family risk, including age at onset, epilepsy localisation and aetiology with a large sample of more than 10 000 probands and 1065/40 544 relatives affected and classified. © 2002 BEA Trading Ltd. Published by Elsevier Science Ltd. All rights reserved

Low ankle-brachial index predicts an adverse 1-year outcome after acute coronary and cerebrovascular events

Background: Low ankle-brachial Index (ABI) identifies patients with symptomatic and asymptomatic peripheral arterial disease. The aim of this study was to correlate ABI value (normal or low) with 1-year clinical outcome in patients hospitalized for acute coronary syndromes or cerebrovascular diseases (CVD). Methods: ABI was measured in consecutive patients hospitalized because of acute myocardial infarction, unstable angina, stroke or transient ischemic attack (TIA). An ABI lower than or equal to 0.90 was considered abnormal. The primary outcome of the study was the composite of non-fatal acute myocardial infarction, non-fatal ischemic stroke, and death from any cause during the year following the index event. Results: An abnormal ABI was found in 27.2% of 1003 patients with acute coronary syndromes, and in 33.5% of 755 patients with acute CVD. After a median follow-up of 372days, the frequency of the primary outcome was 10.8% (57/526) in patients with abnormal ABI and 5.9% (73/1232) in patients with normal ABI [odds ratio (OR) 1.96; 95% CI 1.36-2.81]. Death was more common in patients with abnormal ABI (OR 2.05; 95% CI 1.31-3.22). Cardiovascular mortality accounted for 81.7% of overall mortality. ABI was predictive of adverse outcome after adjustment for vascular risk factors in the logistic regression analysis (OR 1.93; 95% CI 1.24-3.01). The predictive value of ABI was mainly accounted for by patients hospitalized for acute coronary syndromes (adverse outcome: 12.8% in patients with abnormal ABI and 5.9% in patients with normal ABI, OR 2.35; 95% CI 1.47-3.76). Conclusions: An abnormal ABI can be found in one-third of patients hospitalized for acute coronary or cerebrovascular events and is a predictor of an adverse 1-year outcome. \ua9 2006 International Society on Thrombosis and Haemostasis