28 research outputs found
Supersymmetric particle mass measurement with invariant mass correlations
The kinematic end-point technique for measuring the masses of supersymmetric
particles in R-Parity conserving models at hadron colliders is re-examined with
a focus on exploiting additional constraints arising from correlations in
invariant mass observables. The use of such correlations is shown to
potentially resolve the ambiguity in the interpretation of quark+lepton
end-points and enable discrimination between sequential two-body and three-body
lepton-producing decays. The use of these techniques is shown to improve the
SUSY particle mass measurement precision for the SPS1a benchmark model by at
least 20-30% compared to the conventional end-point technique.Comment: 29 pages, 23 .eps figures, JHEP3 style; v2 adds some references and
small clarifications to text; v3 adds some more clarifications to the tex
Supersymmetric particle mass measurement with the boost-corrected contransverse mass
A modification to the contransverse mass (MCT) technique for measuring the
masses of pair-produced semi-invisibly decaying heavy particles is proposed in
which MCT is corrected for non-zero boosts of the centre-of-momentum (CoM)
frame of the heavy states in the laboratory transverse plane. Lack of knowledge
of the mass of the CoM frame prevents exact correction for this boost, however
it is shown that a conservative correction can nevertheless be derived which
always generates an MCT value which is less than or equal to the true value of
MCT in the CoM frame. The new technique is demonstrated with case studies of
mass measurement with fully leptonic ttbar events and with SUSY events
possessing a similar final state.Comment: 33 pages, 33 .eps figures, JHEP3 styl
The Higgs Working Group: Summary Report (2001)
Report of the Higgs working group for the Workshop `Physics at TeV
Colliders', Les Houches, France, 21 May - 1 June 2001. It contains 7 separate
sections: A. Theoretical Developments B. Higgs Searches at the Tevatron C.
Experimental Observation of an invisible Higgs Boson at LHC D. Search for the
Standard Model Higgs Boson using Vector Boson Fusion at the LHC E. Study of the
MSSM channel at the LHC F. Searching for Higgs Bosons in
Production G. Studies of Charged Higgs Boson Signals for the
Tevatron and the LHCComment: 120 pages, latex, many figures, proceedings of the Workshop `Physics
at TeV Colliders', Les Houches, France, 21 May - 1 June 2001, full Author
list included in paper. Typos corrected, author list and acknowledgements
completed. Convernors: D. Cavalli, A. Djouadi, K. Jakobs, A. Nikitenko, M.
Spira, C.E.M. Wagner, W.-M. Ya
Ambient Seismic Noise Image of the Structurally Controlled Heat and Fluid Feeder Pathway at Campi Flegrei Caldera
The TIDES-COST Action (STSM-ES1401-34011) provided a travel grant to framework the research project. The Japan Society for the Promotion of Science - Short-Term Fellowship (JSPS/OF215/022) financed the work, undertaken at Tohoku University and concluded at the University of Aberdeen. We thank Giuseppe Vilardo and Eliana Bellucci Sessa for providing the geomorphological maps, and Simona Petrosino and Paola Cusano for the P- and S-wave pickings used to localise the seismicity. Informal revisions from Guido Ventura, Nick Rawlinson and Chris Kilburn helped us improving the analyses and interpretation, respectively. We acknowledge the help of Naveed Khan in parallelising the codes and two anonymous reviewers who improved the analysis, interpretation, and readibility with their comments. All data to reproduce the maps can be downloaded from the World Data Center PANGAEA data repository, permanent link https://doi.pangaea.de/10.1594/PANGAEA.890238.Peer reviewedPublisher PD
Aurora kinases are expressed in medullary thyroid carcinoma (MTC) and their inhibition suppresses in vitro growth and tumorigenicity of the MTC derived cell line TT
International audienceBACKGROUND: The Aurora kinase family members, Aurora-A, -B and -C, are involved in the regulation of mitosis, and alterations in their expression are associated with cell malignant transformation. To date no information on the expression of these proteins in medullary thyroid carcinoma (MTC) are available. We here investigated the expression of the Aurora kinases in human MTC tissues and their potential use as therapeutic targets. METHODS: The expression of the Aurora kinases in 26 MTC tissues at different TNM stages was analyzed at the mRNA level by quantitative RT-PCR. We then evaluated the effects of the Aurora kinase inhibitor MK-0457 on the MTC derived TT cell line proliferation, apoptosis, soft agar colony formation, cell cycle and ploidy. RESULTS: The results showed the absence of correlation between tumor tissue levels of any Aurora kinase and tumor stage indicating the lack of prognostic value for these proteins. Treatment with MK-0457 inhibited TT cell proliferation in a time- and dose-dependent manner with IC50 = 49.8 ± 6.6 nM, as well as Aurora kinases phosphorylation of substrates relevant to the mitotic progression. Time-lapse experiments demonstrated that MK-0457-treated cells entered mitosis but were unable to complete it. Cytofluorimetric analysis confirmed that MK-0457 induced accumulation of cells with ≥ 4N DNA content without inducing apoptosis. Finally, MK-0457 prevented the capability of the TT cells to form colonies in soft agar. CONCLUSIONS: We demonstrate that Aurora kinases inhibition hampered growth and tumorigenicity of TT cells, suggesting its potential therapeutic value for MTC treatment
Association of kidney disease measures with risk of renal function worsening in patients with type 1 diabetes
Background: Albuminuria has been classically considered a marker of kidney damage progression in diabetic patients and it is routinely assessed to monitor kidney function. However, the role of a mild GFR reduction on the development of stage 653 CKD has been less explored in type 1 diabetes mellitus (T1DM) patients. Aim of the present study was to evaluate the prognostic role of kidney disease measures, namely albuminuria and reduced GFR, on the development of stage 653 CKD in a large cohort of patients affected by T1DM. Methods: A total of 4284 patients affected by T1DM followed-up at 76 diabetes centers participating to the Italian Association of Clinical Diabetologists (Associazione Medici Diabetologi, AMD) initiative constitutes the study population. Urinary albumin excretion (ACR) and estimated GFR (eGFR) were retrieved and analyzed. The incidence of stage 653 CKD (eGFR < 60 mL/min/1.73 m2) or eGFR reduction > 30% from baseline was evaluated. Results: The mean estimated GFR was 98 \ub1 17 mL/min/1.73m2 and the proportion of patients with albuminuria was 15.3% (n = 654) at baseline. About 8% (n = 337) of patients developed one of the two renal endpoints during the 4-year follow-up period. Age, albuminuria (micro or macro) and baseline eGFR < 90 ml/min/m2 were independent risk factors for stage 653 CKD and renal function worsening. When compared to patients with eGFR > 90 ml/min/1.73m2 and normoalbuminuria, those with albuminuria at baseline had a 1.69 greater risk of reaching stage 3 CKD, while patients with mild eGFR reduction (i.e. eGFR between 90 and 60 mL/min/1.73 m2) show a 3.81 greater risk that rose to 8.24 for those patients with albuminuria and mild eGFR reduction at baseline. Conclusions: Albuminuria and eGFR reduction represent independent risk factors for incident stage 653 CKD in T1DM patients. The simultaneous occurrence of reduced eGFR and albuminuria have a synergistic effect on renal function worsening
Tumor necrosis factor (TNF) receptor 1 signaling downstream of TNF receptor-associated factor 2. Nuclear factor kappaB (NFkappaB)-inducing kinase requirement for activation of activating protein 1 and NFkappaB but not of c-Jun N-terminal kinase/stress-activated protein kinase.
Like other members of the tumor necrosis factor (TNF) receptor family, p55 TNF receptor 1 (TNF-R1) lacks intrinsic signaling capacity and transduces signals by recruiting associating molecules. The TNF-R1 associated death domain protein interacts with the p55 TNF-R1 cytoplasmic domain and recruits the Fas-associated death domain protein (which directly activates the apoptotic proteases), the protein kinase receptor interacting protein, and TNF receptor-associated factor 2 (TRAF2). TRAF2 has previously been demonstrated to activate both transcription factor nuclear factor kappaB (NFkappaB) and the c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK) pathway, which in turn stimulates transcription factor activating protein 1 (AP1) mainly via phosphorylation of the c-Jun component. We have investigated the signaling properties of NFkappaB-inducing kinase (NIK), a TRAF2-associated protein kinase that mediates NFkappaB induction. NIK was found to be unable to activate JNK/SAPK, mitogen-activated protein kinase, or p38 kinase. Moreover, NIK was not required for JNK/SAPK activation by TNF-R1, thus representing the first TNF-R1 complex component to dissect the NFkappaB and the JNK/SAPK pathways. Despite being unable to activate JNK/SAPK and mitogen-activated protein kinase, NIK strongly activated AP1 and was required for TNF-R1-induced AP1 activation. Therefore, NIK links TNF-R1 to a novel, JNK/SAPK-independent, AP1 activation pathway