Kamituga: Digital Gold

Questa è una sala espositiva all'interno della più ampia mostra "Planet Digital" (https://www.planetdigital.ch/en) ospitata dal Museum für Gestaltung, Zurigo, Svizzera (dal 20.2.2022 al 6.6.2022

The strong interaction shift and width of the ground state of pionic hydrogen

The 3p-1s transition in pionic hydrogen was investigated with a high-resolution crystal spectrometer system. From the precisely measured transition energy, together with the (calculated) electromagnetic energy, the strong interaction shift of the 1s state was obtained as ϵ1s = −7.127 ± 0.028(stat.)± 0.036(syst.) eV (attractive). From the natural line width, measured for the first time, we determine the decaywidth of the 1s state: Γ1s(decay) = 0.97 ± 0.10(stat.)± 0.05(syst.) eV. With the recently calculated electromagnetic corrections the s-wave scattering lengths of an isospin symmetric strong interaction are deduced. The scattering length for elastic scattering of a negative pion on a proton is aπ−p→π−ph = 0.0885±0.00003(stat.)±0.0006(syst.)mπ−1. The scattering lengthe for single charge exchange is found to be aπ−p→π0nh = −0.136 ± 0.007(stat.) ± 0.003(syst.)mπ−1.The experiment was performed at the Paul Scherrer Institute (PSI) in Switzerland. A focussing crystal spectrometer with an array of bent crystals, the cyclotron trap (a magnetic system designed to increase the particle stop density) and a CCD (charge-coupled device) detector system were employed. The results from the pionic hydrogen experiment — together with those from the pionic deuterium experiment — were used to test the isospin symmetry of the strong interaction. The present data are still consistent with isospin sysmmetry

X-ray spectroscopy of the pionic deuterium atom

The low energy X-rays of the pionic deuterium 3P-1S transition were measured using a high resolution crystal spectrometer, together with a cyclotron trap (a magnetic device to increase the pion stopping density) and a CCD (charge-coupled device) detector system. The spectrometer resolution was 0.65 eV FWHM for a measured energy of approximately 3075 eV. This energy was measured with a precision of 0.1 eV. Compared to conventional methods, the cyclotron trap allowed for a gain in stopping density of about an order of magnitude. The CCDs had excellent spatial and energy resolutions. Non-X-ray background could therefore be almost completely eliminated. The 1S strong interaction shift ϵ1S and total decay width Γ1S were determined from the position and line shape of the X-ray peak. They areϵ1S(shift) = 2.43 ± 0.10eV(repulsive), Γ1S(width) = 1.02 ± 0.21eV, where the statistical and systematic errors were added linearly. The total (complex) pionic deuterium S-wave scattering length aπ−d was deduced:aπ−d= −0.0259(±0.0011) +i0.0054(±0.0011)mπ−1. From the real part of aπ−d a constraint in terms of the isoscalar and isovector πN′ scattering lengths b0 and b1 was deduced. From Im aπ−d we determined the isoscalar coupling constant for π− absorption: |g0| = (2.6 ± 0.3) 10−2mπ−2. The experiments of the pionic hydrogen and deuterium S-wave scattering lengths were analyzed within the framework of a search for i isospin symmetry violation. The data are still compatible with isospin conservation. The scattering lengths deduced from the Karlsruhe-Helsinki phase shift analysis disagree with the present results

A novel class of inhibitors that disrupts the stability of integrin heterodimers identified by CRISPR-tiling-instructed genetic screens

The plasma membrane is enriched for receptors and signaling proteins that are accessible from the extracellular space for pharmacological intervention. Here we conducted a series of CRISPR screens using human cell surface proteome and integrin family libraries in multiple cancer models. Our results identified ITGAV (integrin αV) and its heterodimer partner ITGB5 (integrin β5) as the essential integrin α/β pair for cancer cell expansion. High-density CRISPR gene tiling further pinpointed the integral pocket within the β-propeller domain of ITGAV for integrin αVβ5 dimerization. Combined with in silico compound docking, we developed a CRISPR-Tiling-Instructed Computer-Aided (CRISPR-TICA) pipeline for drug discovery and identified Cpd_AV2 as a lead inhibitor targeting the β-propeller central pocket of ITGAV. Cpd_AV2 treatment led to rapid uncoupling of integrin αVβ5 and cellular apoptosis, providing a unique class of therapeutic action that eliminates the integrin signaling via heterodimer dissociation. We also foresee the CRISPR-TICA approach to be an accessible method for future drug discovery studies