Quantum dynamical phase transition in a system with many-body interactions

We introduce a microscopic Hamiltonian model of a two level system with many-body interactions with an environment whose excitation dynamics is fully solved within the Keldysh formalism. If a particle starts in one of the states of the isolated system, the return probability oscillates with the Rabi frequency $\omega_{0}$. For weak interactions with the environment $1/\tau_{\mathrm{SE}}<2\omega_{0},$ we find a slower oscillation whose amplitude decays with a decoherence rate $1/\tau_{\phi}=1/(2\tau_{\mathrm{SE}})$. However, beyond a finite critical interaction with the environment, $1/\tau_{\mathrm{SE}}>2\omega_{0}$, the decoherence rate becomes $1/\tau_{\phi}\propto(\omega_{0}^{2})\tau_{\mathrm{SE}}$. The oscillation period diverges showing a \emph{quantum dynamical phase transition}to a Quantum Zeno phase.Comment: 5 pages, 3 figures, minor changes, fig.2 modified, added reference

On the estimation of the proportion of sporadic cases in Duchenne muscular dystrophy

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Duchenne muscular dystrophy. Frequency of sporadic cases

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Ethical issue in testing for genetic disease in human

In: Bioethics in research and society. p. 53-56. Lavoro eseguito con il contributo finanziario del Progetto Finalizzato Invecchiamento del Consiglio Nazionale delle Ricerche. Reports presented at the Multidisciplinary Convention entitled 'Bioethics in research and society' organized in October 1992 by the Commission of Bioethics of the CNRConsiglio Nazionale delle Ricerche - Biblioteca Centrale - P.le Aldo Moro, 7, Rome / CNR - Consiglio Nazionale delle RichercheSIGLEITItal

Giovanni Zalin storico dell'economia

Ricostruzione della carriera e del profilo intellettuale di uno storico economico italiano

Duble missense mutation in exon 41 of the human dystrophin gene detected by double strand conformation analysis

Development of late-onset Becker muscular dystrophy is reported in a patient whose two healthy brothers showed high serum creatine kinase level. No cases of neuromuscular disorders had been previously reported in this family. The analysis of the dystrophin gene showed that the three brothers had A-->C transversion at nucleotide 6092 in exon 41, a missense mutation which converts lysine into glutamine. The symptomatic patient showed an additional mutation in the same exon, a T-->C transition at nucleotide 6119, converting a phenylalanine to leucine. The possible pathogenic role of this mutation is discussed

Genetic epidemiology of myotonic dystrophy.

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Italian population data for D1S1656, D3S1358, D8S1132, D10S2325, VWA, FES/FPS, and F13A01.

Allele frequencies for seven STRs loci were obtained from a sample of 215 unrelated healthy Italian individuals