179,427 research outputs found
Z,W bosons.
No full textSi confronttano le previsioni teoriche del Modello Standard elettrodebole iniumale coe risultati degli esperimenti a LEP1 del CERN
The search for CLF violation in the MEG & MEG II experiments
No full textWithin the scope of the Standard Model, the μ+ → e+γ decay is forbidden by lepton flavor conservation. Several lepton flavor violating extensions of the Standard Model however predict a measurable μ+ → e+γ branching ratio. The MEG experiment at PSI presently holds the current best experimental limit for this decay (5.7 × 10^−13 at 90% C.L.) and is currently being upgraded for an improvement of a factor 10 in sensitivity in a time scale of about 4 years. The MEG II upgrade R&D status will be presented, along with the current state of the MEG I data analysi
DNA barcoding and faunistic criteria for a revised taxonomy of Italian Ephemeroptera
No full textThis is the published paper:
Tenchini R, Cardoni S, Piredda R, Simeone MC, Belfiore C (2018) DNA barcoding and faunistic criteria for a revised taxonomy of Italian Ephemeroptera. European Journal of zoology 85, 254-267. DOI:10.1080/24750263.2018.148073
R. BOMBI, Un nuovo anglicismo sintattico?, “Incontri linguistici” 40, 2017, pp. 125-133
No full textSi tratta di una breve presentazione del testo in oggett
Precision Tests of the Electroweak Interaction at the Z Pole
No full textThe measurements of the properties of the Z boson performed with the large data samples collected at LEP and SLC challenge the Standard Model of the Electroweak Interaction with unprecedented precision. This paper reviews the experimental techniques, the measurements and their comparison with theoretical predictions
A. Nardi, La sottotitolazione interlinguistica come strumento di riflessione linguistico-culturale nella formazione accademica – Esempi di trasposizione di realia dal tedesco all’italiano, in R. Calzoni – M. Moroni ed., Passaggi, transiti e contatti tra lingue e culture: la traduzione e la germanistica italiana, “Studi Germanici – Quaderni dell’AIG”, 15, 2019, supplemento, pp. 119- 136
No full textBreve presentazione del testo in oggett
Coagulation factor V
No full textThe coagulation cascade involves sequential enzymatic activations of serine protease zymogens that converge on the generation of thrombin. Factor V (FV) takes part in this process as a component of the prothrombinase complex. Besides its role as procoagulant factor, it is also involved in the physiologic anticoagulant pathway, by participating in the inactivation of activated factor VIII (FVIIIa). Given the dual role of FV, genetic defects in FV gene may result in opposite hemorrhagic or thrombotic phenotypes. This review focuses on the structure, function (procoagulant and anticoagulant), regulation (activation and inactivation) of FV as well as on the genetic defects associated with mutations in the FV gene
Inherited defects of coagulation factor V : the hemorrhagic side
No full textCoagulation factor V (FV) is the protein cofactor required in vivo for the rapid generation of thrombin catalyzed by the prothrombinase complex. It also represents a central regulator in the early phases of blood clot formation, as it contributes to the anticoagulant pathway by participating in the downregulation of factor VIII activity. Conversion of precursor FV to either a procoagulant or anticoagulant cofactor depends on the local concentration of procoagulant and anticoagulant enzymes, so that FV may be regarded as a daring tight-rope walker gently balancing opposite forces. Given this dual role, genetic defects in the FV gene may result in opposite phenotypes (hemorrhagic or thrombotic). Besides a concise description on the structural, procoagulant and anticoagulant properties of FV, this review will focus on bleeding disorders associated with altered levels of this molecule. Particular attention will be paid to the mutational spectrum of type I FV deficiency, which is characterized by a remarkable genetic heterogeneity and by an uneven distribution of mutations throughout the FV gene
The molecular basis of quantitative fibrinogen disorders
No full textHereditary fibrinogen disorders include type I deficiencies (afibrinogenemia and hypofibrinogenemia, i.e. quantitative defects), with low or unmeasurable levels of immunoreactive protein; and type II deficiencies (dysfibrinogenemia and hypodysfibrinogenemia, i.e. qualitative defects), showing normal or altered antigen levels associated with reduced coagulant activity. While dysfibrinogenemias are in most cases autosomal dominant disorders, type I deficiencies are generally inherited as autosomal recessive traits. Patients affected by congenital afibrinogenemia or severe hypofibrinogenemia may experience bleeding manifestations varying from mild to severe. This review focuses on the genetic bases of type I fibrinogen deficiencies, which are invariantly represented by mutations within the three fibrinogen genes (FGA, FGB, and FGG) coding for the three polypeptide chains Aalpha, Bbeta, and gamma. From the inspection of the mutational spectrum of these disorders, some conclusions can be drawn: (i) genetic defects are scattered throughout the three fibrinogen genes, with only few sites appearing to represent relative mutational hot spots; (ii) several different types of genetic lesions and pathogenic mechanisms have been described in affected individuals (including gross deletions, point mutations causing premature termination codons, missense mutations affecting fibrinogen assembly/secretion, and uniparental isodisomy associated with a large deletion); (iii) the possibility to express recombinant fibrinogen mutants in eukaryotic cells is rapidly shedding light into the molecular mechanisms responsible for physiologic and pathologic properties of the molecule; (iv) though mutation analysis of the fibrinogen cluster does not yield precise information for predicting genotype/phenotype correlations, it still provides a valuable tool for diagnosis confirmation, identification of potential carriers, and prenatal diagnosis
A multi-act perspective on slurs
No full textThis paper proposes a semantic interpretation of slurs based on a multi-speech act theory. According to this perspective, when a speaker utters a sentence containing a slur, he or she performs two different speech acts, one of which, following Searle’s taxonomy, is an expressive one. Therefore, slurs have two semantic components, the first being identical with the intension and extension of the corresponding neutral term. The second is an expressive speech act by means of which the speaker expresses derogation and denigration towards the class of individuals designated by the neutral component. This interpretation is in line with those theories which regard slurs as having a mixed semantics. However, unlike these theories, in this proposal slurs are not regarded as a type of conventional implicature
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