21 research outputs found
Differential branching fraction and angular analysis of decays
The differential branching fraction of the rare decay is measured as a function of , the
square of the dimuon invariant mass. The analysis is performed using
proton-proton collision data, corresponding to an integrated luminosity of 3.0
\mbox{ fb}^{-1}, collected by the LHCb experiment. Evidence of signal is
observed in the region below the square of the mass. Integrating
over 15 < q^{2} < 20 \mbox{ GeV}^2/c^4 the branching fraction is measured as
d\mathcal{B}(\Lambda^{0}_{b} \rightarrow \Lambda \mu^+\mu^-)/dq^2 = (1.18 ^{+
0.09} _{-0.08} \pm 0.03 \pm 0.27) \times 10^{-7} ( \mbox{GeV}^{2}/c^{4})^{-1},
where the uncertainties are statistical, systematic and due to the
normalisation mode, , respectively.
In the intervals where the signal is observed, angular distributions are
studied and the forward-backward asymmetries in the dimuon ()
and hadron () systems are measured for the first time. In the
range 15 < q^2 < 20 \mbox{ GeV}^2/c^4 they are found to be A^{l}_{\rm FB} =
-0.05 \pm 0.09 \mbox{ (stat)} \pm 0.03 \mbox{ (syst)} and A^{h}_{\rm FB} =
-0.29 \pm 0.07 \mbox{ (stat)} \pm 0.03 \mbox{ (syst)}.Comment: 27 pages, 10 figures, Erratum adde
Differential branching fraction and angular analysis of Lambda(0)(b) -> Lambda mu(+)mu(-) decays
The differential branching fraction of the rare decay is measured as a function of , the
square of the dimuon invariant mass. The analysis is performed using
proton-proton collision data, corresponding to an integrated luminosity of 3.0
\mbox{ fb}^{-1}, collected by the LHCb experiment. Evidence of signal is
observed in the region below the square of the mass. Integrating
over 15 < q^{2} < 20 \mbox{ GeV}^2/c^4 the branching fraction is measured as
d\mathcal{B}(\Lambda^{0}_{b} \rightarrow \Lambda \mu^+\mu^-)/dq^2 = (1.18 ^{+
0.09} _{-0.08} \pm 0.03 \pm 0.27) \times 10^{-7} ( \mbox{GeV}^{2}/c^{4})^{-1},
where the uncertainties are statistical, systematic and due to the
normalisation mode, , respectively.
In the intervals where the signal is observed, angular distributions are
studied and the forward-backward asymmetries in the dimuon ()
and hadron () systems are measured for the first time. In the
range 15 < q^2 < 20 \mbox{ GeV}^2/c^4 they are found to be A^{l}_{\rm FB} =
-0.05 \pm 0.09 \mbox{ (stat)} \pm 0.03 \mbox{ (syst)} and A^{h}_{\rm FB} =
-0.29 \pm 0.07 \mbox{ (stat)} \pm 0.03 \mbox{ (syst)}.Comment: 27 pages, 10 figures, Erratum adde
Rare mendelian primary immunodeficiency diseases associated with impaired NF-ÎșB signaling
Mendelian primary immunodeficiency diseases (MPIDs) are rare disorders affecting distinct constituents of the innate and adaptive immune system. Although they are genetically heterogeneous, a substantial group of MPIDs is due to mutations in genes affecting the nuclear factor-ÎșB (NF-ÎșB) transcription pathway, essential for cell proliferation and cell survival and involved in innate immunity and inflammation. Many of these genes encode for crucial regulatory components of the NF-ÎșB pathway and their mutations are associated with immunological and developmental signs somehow overlapping in patients with MPIDs. At present, nine different MPIDs listed in the online mendelian inheritance in man (OMIM) are caused by mutations in at least nine different genes strictly involved in the NF-ÎșB pathway that result in defects in immune responses. Here we report on the distinct function of each causative gene, on the impaired NF-ÎșB step and more in general on the molecular mechanisms underlining the pathogenesis of the disease. Overall, the MPIDs affecting the NF-ÎșB signalosome require a careful integrated diagnosis and appropriate genetic tests to be molecularly identified. Their discovery at an ever-increasing rate will help establish a common therapeutic strategy for a subclass of immunodeficient patients