Tau | EPFL Graph Search

Tau (capitale Τ, minuscule τ ; en grec ταυ) est la lettre de l'alphabet grec, précédée par sigma et suivie par upsilon. Dérivée de la lettre tau x12px|tau de l'alphabet phénicien, elle est l'ancêtre de la lettre T de l'alphabet latin et de la lettre Т de l'alphabet cyrillique. Caractéristiques Usage En grec moderne comme en grec ancien, la lettre tau représente la consonne occlusive alvéolaire sourde (). Dans le système de numération grecque, tau vaut 300 ; par exemple représente le nombre 300. Comme la plupart des autres lettres grecques, le tau est parfois utilisé en dehors de son contexte alphabétique grec dans les sciences. τ sert par exemple en physique à noter un temps relatif (un temps de réponse, par exemple), quand le caractère t est utilisé pour le temps absolu. Tau est aussi utilisé dans le domaine des mathématiques, c'est la lettre grecque utilisée pour dire : Topologie. En physique, il existe également le lepton Tau (ou tauon). En médecine, Tau

Measurement of lifetimes for heavy flavour mesons using semileptonic B decays at LHCb

Brice Emile Maurin

This thesis work presents lifetime measurements of heavy-flavour mesons made with semileptonic

B^0

and

B^0_s

decays based on

3~{\rm fb}^{-1}

of data collected with the LHCb detector in proton-proton collisions at centre-of-mass energies of 7 and 8 TeV. The study of meson lifetimes is important to constrain phenomenological models for hadronic interactions based on the Standard Model of particle physics. Better understanding of hadronic interactions is essential for making precise predictions, which can then be confronted to experimental data in order to look for signs of physics beyond the Standard Model. We measure the differences between the decay widths of the

B^0_s

and

B^0

mesons,

\Delta(B)

, and between that of the

D_s^-

and

D^-

mesons,

\Delta(D)

, by analysing approximately 410000

B^0_s \to D_{s}^{(*)-}\mu^{+}\nu_{\mu}

and 110000

B^0 \to D^{(*)-}\mu^{+}\nu_{\mu}

decays, which are partially reconstructed in the same

K^+K^-\pi^-\mu^+

final state. We measure

\Delta(B) = -0.0115 \pm 0.0053~{\rm(stat)} \pm 0.0041~{\rm(syst)}~{\rm ps}^{-1}

and

\Delta(D) = 1.0131 \pm 0.0117~{\rm(stat)} \pm 0.0065~{\rm(syst)}~{\rm ps}^{-1}.

Using the obtained values of

\Delta(D)

and

\Delta(B)

and the

B^0

and

D^-

lifetimes as external inputs, we obtain a measurement of the flavour-specific

B^0_s

lifetime,

\tau_s^{\rm fs} = 1.547 \pm 0.013~{\rm(stat)} \pm 0.010~{\rm (syst)} \pm 0.004~{\rm(\tau_{B^0})}~{\rm ps},

and of the

D_s^-

lifetime,

\tau_{D_s^-} = 0.5064 \pm 0.0030~{\rm(stat)} \pm 0.0017~{\rm (syst)} \pm 0.0017~{\rm(\tau_{D^-})}~{\rm ps},

where the last uncertainties originate from the limited knowledge of the

B^0

and

D^-

lifetimes, respectively. Both results are compatible with, and improve upon, previous determinations. A feasibility study of a

D^0

lifetime measurement is performed, by measuring the difference between the decay widths of the

D^0

and

D^-

mesons,

\Delta(D)'

. We reconstruct approximately

2.2\times 10^6

B^0\to D^{*-}(\to \bar{D}^0 (\to K^+\pi^-)\pi^-)\mu^+\nu_{\mu}

and

1.6\times 10^6

B^0\to D^{(*)-}(\to K^+\pi^-\pi^- (X))\mu^+\nu_{\mu}

decays. We measure

\Delta(D)' = 1.4644 \pm 0.0043~{\rm(stat)} \pm 0.0132~{\rm(syst)}~{\rm ps}^{-1}

and with the

D^-

lifetime as external input, we get an estimate of the

D^0

lifetime,

\tau_{D^0} = 0.4122 \pm 0.0007~{\rm(stat)} \pm 0.0022~{\rm (syst)} \pm 0.0011~{\rm(\tau_{D^-})}~{\rm ps}.

This result is compatible with, but less precise than, current precision and thus validates the method. We discuss possible improvements with larger simulation samples and data sets.

EPFL2018

Conditional expression of Parkinson's disease-related R1441C LRRK2 in midbrain dopaminergic neurons of mice causes nuclear abnormalities without neurodegeneration

Shi-Yan Caroline Foo, Liliane Glauser, Meghna Kannan, Graham Knott, Darren Moore, Elpida Tsika

Mutations in the leucine-rich repeat kinase 2 (LRRK2) gene cause late-onset, autosomal dominant Parkinson's disease (PD). The clinical and neurochemical features of LRRK2-linked PD are similar to idiopathic disease although neuropathology is somewhat heterogeneous. Dominant mutations in LRRK2 precipitate neurodegeneration through a toxic gain-of-function mechanism which can be modeled in transgenic mice overexpressing human LRRK2 variants. A number of LRRK2 transgenic mouse models have been developed that display abnormalities in dopaminergic neurotransmission and alterations in tau metabolism yet without consistently inducing dopaminergic neurodegeneration. To directly explore the impact of mutant LRRK2 on the nigrostriatal dopaminergic pathway, we developed conditional transgenic mice that selectively express human R1441C LRRK2 in dopaminergic neurons from the endogenous murine ROSA26 promoter. The expression of R1441C LRRK2 does not induce the degeneration of substantia nigra dopaminergic neurons or striatal dopamine deficits in mice up to 2 years of age, and fails to precipitate abnormal protein inclusions containing alpha-synuclein, tau, ubiquitin or autophagy markers (LC3 and p62). Furthermore, mice expressing R1441C LRRK2 exhibit normal motor activity and olfactory function with increasing age. Intriguingly, the expression of R1441C LRRK2 induces age-dependent abnormalities of the nuclear envelope in nigral dopaminergic neurons including reduced nuclear circularity and increased invaginations of the nuclear envelope. In addition, R1441C LRRK2 mice display increased neurite complexity of cultured midbrain dopaminergic neurons. Collectively, these novel R1441C LRRK2 conditional transgenic mice reveal altered dopaminergic neuronal morphology with advancing age, and provide a useful tool for exploring the pathogenic mechanisms underlying the R1441C LRRK2 mutation in PD. (C) 2014 Elsevier Inc All rights reserved.

Elsevier2014

Measurement of lifetimes for heavy flavour mesons using semileptonic B decays at LHCb

Brice Emile Maurin

This thesis work presents lifetime measurements of heavy-flavour mesons made with semileptonic

B^0

and

B^0_s

decays based on

3~{\rm fb}^{-1}

B^0_s

and

B^0

mesons,

\Delta(B)

, and between that of the

D_s^-

and

D^-

mesons,

\Delta(D)

, by analysing approximately 410000

B^0_s \to D_{s}^{(*)-}\mu^{+}\nu_{\mu}

and 110000

B^0 \to D^{(*)-}\mu^{+}\nu_{\mu}

decays, which are partially reconstructed in the same

K^+K^-\pi^-\mu^+

final state. We measure

\Delta(B) = -0.0115 \pm 0.0053~{\rm(stat)} \pm 0.0041~{\rm(syst)}~{\rm ps}^{-1}

and

\Delta(D) = 1.0131 \pm 0.0117~{\rm(stat)} \pm 0.0065~{\rm(syst)}~{\rm ps}^{-1}.

Using the obtained values of

\Delta(D)

and

\Delta(B)

and the

B^0

and

D^-

lifetimes as external inputs, we obtain a measurement of the flavour-specific

B^0_s

lifetime,

\tau_s^{\rm fs} = 1.547 \pm 0.013~{\rm(stat)} \pm 0.010~{\rm (syst)} \pm 0.004~{\rm(\tau_{B^0})}~{\rm ps},

and of the

D_s^-

lifetime,

\tau_{D_s^-} = 0.5064 \pm 0.0030~{\rm(stat)} \pm 0.0017~{\rm (syst)} \pm 0.0017~{\rm(\tau_{D^-})}~{\rm ps},

where the last uncertainties originate from the limited knowledge of the

B^0

and

D^-

lifetimes, respectively. Both results are compatible with, and improve upon, previous determinations. A feasibility study of a

D^0

lifetime measurement is performed, by measuring the difference between the decay widths of the

D^0

and

D^-

mesons,

\Delta(D)'

. We reconstruct approximately

2.2\times 10^6

B^0\to D^{*-}(\to \bar{D}^0 (\to K^+\pi^-)\pi^-)\mu^+\nu_{\mu}

and

1.6\times 10^6

B^0\to D^{(*)-}(\to K^+\pi^-\pi^- (X))\mu^+\nu_{\mu}

decays. We measure

\Delta(D)' = 1.4644 \pm 0.0043~{\rm(stat)} \pm 0.0132~{\rm(syst)}~{\rm ps}^{-1}

and with the

D^-

lifetime as external input, we get an estimate of the

D^0

lifetime,

\tau_{D^0} = 0.4122 \pm 0.0007~{\rm(stat)} \pm 0.0022~{\rm (syst)} \pm 0.0011~{\rm(\tau_{D^-})}~{\rm ps}.

This result is compatible with, but less precise than, current precision and thus validates the method. We discuss possible improvements with larger simulation samples and data sets.

EPFL2018

Conditional expression of Parkinson's disease-related R1441C LRRK2 in midbrain dopaminergic neurons of mice causes nuclear abnormalities without neurodegeneration

Shi-Yan Caroline Foo, Liliane Glauser, Meghna Kannan, Graham Knott, Darren Moore, Elpida Tsika

Elsevier2014