Publications by authors named "K R Mattioli"
Article Synopsis
- The study investigates CP symmetry violation in the decay of D^{+} particles into K^{-}K^{+}π^{+} using data from proton-proton collisions at a high energy of 13 TeV.
- A unique model-independent method was employed to analyze the phase-space distributions of D^{+} and D^{-} particles, correcting for any instrumental biases using D_{s}^{+} decays.
- The findings indicate no significant evidence of CP violation, with a p value of 8.1%, and measure specific CP asymmetry observables, marking this study as the most sensitive search of its kind in multibody decays.
Article Synopsis
- A study was conducted on B^{+} decays to explore resonant structures using data from the LHCb experiment at various energy levels, totaling an integrated luminosity of 9 fb^{-1}.
- The researchers performed a simultaneous amplitude fit on two decay channels, determining the C parities of resonances in the D^{*±}D^{∓} mass spectra.
- Four new charmonium or charmoniumlike states were discovered, including η_{c}(3945) and h_{c}(4000), and the presence of T_{c[over ¯]s[over ¯]0}^{*}(2870)^{0} and T_{c[over ¯]s
Triple-negative breast cancer (TNBC) is the most aggressive breast cancer subtype and has the highest rate of recurrence. The predominant standard of care for advanced TNBC is systemic chemotherapy with or without immunotherapy; however, responses are typically short lived. Thus, there is an urgent need to develop more effective treatments.
View Article and Find Full Text PDFA measurement of time-dependent CP violation in D^{0}→π^{+}π^{-}π^{0} decays using a pp collision data sample collected by the LHCb experiment in 2012 and from 2015 to 2018, corresponding to an integrated luminosity of 7.7 fb^{-1}, is presented. The initial flavor of each D^{0} candidate is determined from the charge of the pion produced in the D^{*}(2010)^{+}→D^{0}π^{+} decay.
View Article and Find Full Text PDFCombined EZH2 and RAS pathway inhibitors kill KRAS-mutant colorectal cancer cells and promote durable tumor regression in vivo. These agents function by cooperatively suppressing the WNT pathway, driving differentiation, and epigenetically reprogramming cells to permit the induction of apoptotic signals, which then kill these more differentiated tumor cells.
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