Using a neural network approach for muon reconstruction and triggering

The extremely high rate of events that will be produced in the future Large Hadron Collider requires the triggering mechanism to take precise decisions in a few nano-seconds. We present a study which used an artificial neural network triggering algorithm and compared it to the performance of a dedicated electronic muon triggering system. Relatively simple architecture was used to solve a complicated inverse problem. A comparison with a realistic example of the ATLAS first level trigger simulation was in favour of the neural network. A similar architecture trained after the simulation of the electronics first trigger stage showed a further background rejection.Comment: A talk given at ACAT03, KEK, Japan, November 2003. Submitted to Nuclear Instruments and Methods in Physics Research, Section

PCNA Ubiquitination Is Important, But Not Essential for Translesion DNA Synthesis in Mammalian Cells

Translesion DNA synthesis (TLS) is a DNA damage tolerance mechanism in which specialized low-fidelity DNA polymerases bypass replication-blocking lesions, and it is usually associated with mutagenesis. In Saccharomyces cerevisiae a key event in TLS is the monoubiquitination of PCNA, which enables recruitment of the specialized polymerases to the damaged site through their ubiquitin-binding domain. In mammals, however, there is a debate on the requirement for ubiquitinated PCNA (PCNA-Ub) in TLS. We show that UV-induced Rpa foci, indicative of single-stranded DNA (ssDNA) regions caused by UV, accumulate faster and disappear more slowly in Pcna(K164R/K164R) cells, which are resistant to PCNA ubiquitination, compared to Pcna(+/+) cells, consistent with a TLS defect. Direct analysis of TLS in these cells, using gapped plasmids with site-specific lesions, showed that TLS is strongly reduced across UV lesions and the cisplatin-induced intrastrand GG crosslink. A similar effect was obtained in cells lacking Rad18, the E3 ubiquitin ligase which monoubiquitinates PCNA. Consistently, cells lacking Usp1, the enzyme that de-ubiquitinates PCNA exhibited increased TLS across a UV lesion and the cisplatin adduct. In contrast, cells lacking the Rad5-homologs Shprh and Hltf, which polyubiquitinate PCNA, exhibited normal TLS. Knocking down the expression of the TLS genes Rev3L, PolH, or Rev1 in Pcna(K164R/K164R) mouse embryo fibroblasts caused each an increased sensitivity to UV radiation, indicating the existence of TLS pathways that are independent of PCNA-Ub. Taken together these results indicate that PCNA-Ub is required for maximal TLS. However, TLS polymerases can be recruited to damaged DNA also in the absence of PCNA-Ub, and perform TLS, albeit at a significantly lower efficiency and altered mutagenic specificity

Exact Analytic Solution for the Rotation of a Rigid Body having Spherical Ellipsoid of Inertia and Subjected to a Constant Torque

The exact analytic solution is introduced for the rotational motion of a rigid body having three equal principal moments of inertia and subjected to an external torque vector which is constant for an observer fixed with the body, and to arbitrary initial angular velocity. In the paper a parametrization of the rotation by three complex numbers is used. In particular, the rows of the rotation matrix are seen as elements of the unit sphere and projected, by stereographic projection, onto points on the complex plane. In this representation, the kinematic differential equation reduces to an equation of Riccati type, which is solved through appropriate choices of substitutions, thereby yielding an analytic solution in terms of confluent hypergeometric functions. The rotation matrix is recovered from the three complex rotation variables by inverse stereographic map. The results of a numerical experiment confirming the exactness of the analytic solution are reported. The newly found analytic solution is valid for any motion time length and rotation amplitude. The present paper adds a further element to the small set of special cases for which an exact solution of the rotational motion of a rigid body exists.Comment: "Errata Corridge Postprint" In particular: typos present in Eq. 28 of the Journal version are HERE correcte

Exact Analytic Solutions for the Rotation of an Axially Symmetric Rigid Body Subjected to a Constant Torque

New exact analytic solutions are introduced for the rotational motion of a rigid body having two equal principal moments of inertia and subjected to an external torque which is constant in magnitude. In particular, the solutions are obtained for the following cases: (1) Torque parallel to the symmetry axis and arbitrary initial angular velocity; (2) Torque perpendicular to the symmetry axis and such that the torque is rotating at a constant rate about the symmetry axis, and arbitrary initial angular velocity; (3) Torque and initial angular velocity perpendicular to the symmetry axis, with the torque being fixed with the body. In addition to the solutions for these three forced cases, an original solution is introduced for the case of torque-free motion, which is simpler than the classical solution as regards its derivation and uses the rotation matrix in order to describe the body orientation. This paper builds upon the recently discovered exact solution for the motion of a rigid body with a spherical ellipsoid of inertia. In particular, by following Hestenes' theory, the rotational motion of an axially symmetric rigid body is seen at any instant in time as the combination of the motion of a "virtual" spherical body with respect to the inertial frame and the motion of the axially symmetric body with respect to this "virtual" body. The kinematic solutions are presented in terms of the rotation matrix. The newly found exact analytic solutions are valid for any motion time length and rotation amplitude. The present paper adds further elements to the small set of special cases for which an exact solution of the rotational motion of a rigid body exists.Comment: "Errata Corridge Postprint" version of the journal paper. The following typos present in the Journal version are HERE corrected: 1) Definition of \beta, before Eq. 18; 2) sign in the statement of Theorem 3; 3) Sign in Eq. 53; 4)Item r_0 in Eq. 58; 5) Item R_{SN}(0) in Eq. 6

Familial Mediterranean Fever and Hyperimmunoglobulinemia D syndrome: two diseases with distinct clinical, serologic, and genetic features

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Familial Mediterranean fever, Inflammation and Nephrotic Syndrome: Fibrillary Glomerulopathy and the M680I Missense Mutation

BACKGROUND: Familial Mediterranean fever (FMF) is an autosomal recessive disease characterized by inflammatory serositis (fever, peritonitis, synovitis and pleuritis). The gene locus responsible for FMF was identified in 1992 and localized to the short arm of chromosome 16. In 1997, a specific FMF gene locus, MEFV, was discovered to encode for a protein, pyrin that mediates inflammation. To date, more than forty missense mutations are known to exist. The diversity of mutations identified has provided insight into the variability of clinical presentation and disease progression. CASE REPORT: We report an individual heterozygous for the M680I gene mutation with a clinical diagnosis of FMF using the Tel-Hashomer criteria. Subsequently, the patient developed nephrotic syndrome with biopsy-confirmed fibrillary glomerulonephritis (FGN). Further diagnostic studies were unremarkable with clinical workup negative for amyloidosis or other secondary causes of nephrotic syndrome. DISCUSSION: Individuals with FMF are at greater risk for developing nephrotic syndrome. The most serious etiology is amyloidosis (AA variant) with renal involvement, ultimately progressing to end-stage renal disease. Other known renal diseases in the FMF population include IgA nephropathy, IgM nephropathy, Henoch-Schönlein purpura as well as polyarteritis nodosa. CONCLUSION: To our knowledge, this is the first association between FMF and the M680I mutation later complicated by nephrotic syndrome and fibrillary glomerulonephritis