Reconstruction of semileptonically decaying beauty hadrons produced in high energy pp collisions

It is well known that in $b$ hadron decays with a single unreconstructible final state particle, the decay kinematics can be solved up to a quadratic ambiguity, without any knowledge of the $b$ hadron momentum. We present a method to infer the momenta of $b$ hadrons produced in hadron collider experiments using information from their reconstructed flight vectors. Our method is strictly agnostic to the decay itself, which implies that it can be validated with control samples of topologically similar decays to fully reconstructible final states. A multivariate regression algorithm based on the flight information provides a $b$ hadron momentum estimate with a resolution of around 60% which is sufficient to select the correct solution to the quadratic equation in around 70% of cases. This will improve the ability of hadron collider experiments to make differential decay rate measurements with semileptonic $b$ hadron decays.Comment: 18 pages, 17 figures. Updated version to be published in JHE

A model for the development of types of atolls and volcanic islands on the Pacific lithospheric plate

"This paper is an expansion of a paper first delivered to the Annual Meeting of the Association of Canadian Geographers at Laval University, Quebec, May 1976."A literature review on atoll origins and volcanic island development on the Pacific lithospheric plate is combined with bathymetric data on the Hawaiian, Marshall, Caroline, Tuamotu and Society island chains to produce a model which helps explain the development of all major Pacific plate island types. This model incorporates the concept that as new lithosphere is formed along the East Pacific Rise older crust moves north-west towards Asia, cools and causes ocean deepening. Some distance from the East Pacific Rise relatively fixed melting anomalies produce volcanic island chains. In warmer waters these islands develop fringing reefs which continue to grow to wave level as the islands are carried on the cooling plate into deeper water. Raised volcanic island forms can develop on arches produced by the isostatic subsidence of new magmatic outpourings close by. As volcanic islands with fringing reefs move into deeper water almost-atolls and finally true atolls develop. Partly raised and raised forms result if atolls rise over minor upwarps on the crust produced by, 1) asthenospheric bumps, 2) arch flexuring resulting from isostatic subsidence of nearby magmatic outpourings, 3) compression within the lithosphere alongside Pacific plate subduction zones. The model also helps explain certain types of drowned atolls and guyots."Financial assistance from the University of Winnipeg is acknowledged.

Muscle biopsy and cell cultures: potential diagnostic tools in hereditary skeletal muscle channelopathies.

Hereditary muscle channelopathies are caused by dominant mutations in the genes encoding for subunits of muscle voltage- gated ion channels. Point mutations on the human skeletal muscle Na+ channel (Nav1.4) give rise to hyperkalemic periodic paralysis, potassium aggravated myotonia, paramyotonia congenita and hypokalemic periodic paralysis type 2. Point mutations on the human skeletal muscle Ca2+ channel give rise to hypokalemic periodic paralysis and malignant hyperthermia. Point mutations in the human skeletal chloride channel ClC-1 give rise to myotonia congenita. Point mutations in the inwardly rectifying K+ channel Kir2.1 give rise to a syndrome characterized by periodic paralysis, severe cardiac arrhythmias and skeletal alterations (Andersen's syndrome). Involvement of the same ion channel can thus give rise to different phenotypes. In addition, the same mutation can lead to different phenotypes or similar phenotypes can be caused by different mutations on the same or on different channel subtypes. Bearing in mind, the complexity of this field, the growing number of potential channelopathies (such as the myotonic dystrophies), and the time and cost of the genetic procedures, before a biomolecular approach is addressed, it is mandatory to apply strict diagnostic protocols to screen the patients. In this study we propose a protocol to be applied in the diagnosis of the hereditary muscle channelopathies and we demonstrate that muscle biopsy studies and muscle cell cultures may significantly contribute towards the correct diagnosis of the channel involved. DNAbased diagnosis is now a reality for many of the channelopathies. This has obvious genetic counselling, prognostic and therapeutic implications

Biomolecular identification of (CCTG)n mutation in myotonic dystrophy type 2 (DM2) by FISH on muscle biopsy

Myotonic dystrophy type 2 (DM2) is a dominantly inherited disorder with multisystemic clinical features, caused by a CCTG repeat expansion in intron 1 of the zinc finger protein 9 (ZNF9) gene. The mutant transcripts are retained in the nucleus forming multiple discrete foci also called ribonuclear inclusions. The size and the somatic instability of DM2 expansion complicate the molecular diagnosis of DM2. In our study fluorescence-labeled CAGG-repeat oligonucleotides were hybridized to muscle biopsies to investigate if fluorescence in situ hybridization (FISH), a relatively quick and simple procedure, could be used as a method to diagnose DM2. When FISH was performed with (CAGG)5 probe, nuclear foci of mutant RNA were present in all genetically confirmed DM2 patients (n = 17) and absent in all patients with myotonic dystrophy type 1 (DM1; n = 5) or with other muscular disease (n = 17) used as controls. In contrast, foci were observed both in DM1 and DM2 myonuclei when muscle tissue were hybridized with (CAG)6CA probe indicating that this probe is not specific for DM2 identification. The consistent detection of ribonuclear inclusions in DM2 muscles and their absence in DM1, in agreement with the clinical diagnosis and with leukocyte (CCTG)n expansion, suggests that fluorescence in situ hybridization using (CAGG)5 probes, may be a specific method to distinguish between DM1 and DM2. Moreover, the procedure is simple, and readily applicable in any pathology laboratory

Upgrade of the L2 electronics in the CMS Muon Drift Tubes system

The excellent performance of the DT system during the past years is expected to be pursued at the increased luminosity, so the main motivation driving the DT upgrade is focused on improving the electronic system to maintain its reliability. The fulfillment of this project envisages to turn electrical signals into optical signals for a total number of 3500 optical channels that run at up to 480 Mb/s data rate. A Bit Error Rate (BER) of the order of 10−12 with a confidence level (CL) of 95% has been measured which ensures that an appropriate components choice has been made in view of the full boards production

Test results of the front-end system for the Silicon Drift Detectors of ALICE

The front-end system of the Silicon Drift Detectors (SDDs) of the ALICE experiment is made of two ASICs. The first chip performs the preamplification, temporary analogue storage and analogue-to-digital conversion of the detector signals. The second chip is a digital buffer that allows for a significant reduction of the connection from the front-end module to the outside world. In this paper, the results achieved on the first complete prototype of the front-end system for the SDDs of ALICE are presented

Human exonuclease 1 role in response to UV irradiation

DNA damage checkpoints are surveillance mechanisms that monitor the integrity of the genome. Nucleotide excision repair (NER) is a DNA repair mechanism that cells use to remove UV-induced DNA lesions. Previous publication from our laboratory demonstrated that recognition and processing of UV-induced damage by NER is required for proper activation of checkpoint through interactions between NER proteins and checkpoint factors in yeast and human primary fibroblasts. From a two hybrid screening in yeast exonuclease 1 (Exo1) was identified as a 9-1-1 complex interactor. Exo1 is a 5\u2019-3\u2019 exonuclease and 5'-flap-endonuclease with many different roles in DNA metabolism such as meiotic and mitotic recombination, mismatch repair and telomere processing. Characterization of an exo1 yeast deleted strain has shown that this protein is involved in the early steps of UV-induced DNA damage checkpoint. In human cells EXO1 is present as two isoforms named hEXO1a and hEXO1b genetarated by alternative splicing. We are analyzing the role of EXO1 in checkpoint activation in response to UV-C damage in human cells: using siRNA against both a and b isoform of hEXO1 in G1 cells we were able to observe a defect in Chk1 and p53 phosphorylation induced by UV-C irradiation

Mutation in the S4 segment of the adult skeletal sodium channel gene in an Italian paramyotonia congenita (PC) family

The periodic paralyses are a group of autosomal dominant muscle diseases sharing the common feature of episodic stiffness and weakness, usually occurring with muscle cooling (as in the case of paramyotonia congenita, PC pheno-type) or changes in extracellular K+ levels resulting from various precipitating factors (hyperkalemic periodic paralysis, HYPP and hypokalemic periodic paralysis, Hypo PP). It is now known that HYPP maps to chromosome 17q, and that PC and a form of myotonia congenita without periodic paralysis also map to the 17q locus, thus indicating that they derive from allelic variants. So far, these disorders have been described in various ethnic groups but, to our knowledge, have never been reported in Italy. We describe a mutation in an S4 segment of the adult skeletal muscle sodium channel in a clinically-defined Italian family that leads to the paramyotonia congenita (PC) phenotype with dominant autosomal inheritance and temperature-related symptoms (regional weakness following cooling and exercise), present since childhood in all of the affected family members