Phenomenological model for the Kbar N --> K Xi reaction

A phenomenological model for the Kbar N --> K Xi reaction is suggested. The model includes s and u channel exchanges by Lambda, Sigma, Sigma(1385), and Lambda(1520) and s channel exchanges by above-threshold hyperonic resonances. Explicit expression for the propagator for a particle with spin 7/2 is presented. High-mass and high-spin resonances play a significant role in the process. We deal with the whole set of existing experimental data on the cross sections and polarizations in the energy range from the threshold to 2.8 GeV in the center-of-mass system and reach a good agreement with experiments. Applications of the model to other elementary reactions of Xi production and to Xi hypernuclear spectroscopy are briefly discussed.Comment: Published version; minor change

Measurement of the Xi0 -> Lambda gamma Decay Asymmetry and Branching Fraction

In data taken with the NA48 experiment at the CERN SPS in 1999, 730 candidates of the weak radiative hyperon decay Xi0 -> Lambda gamma have been found with an estimated background of 58+-8 events. From these events the Xi0 -> Lambda gamma decay asymmetry has been determined to alpha(Xi0 -> Lambda gamma) = -0.78 +- 0.18_stat +- 0.06_syst, which is the first evidence of a decay asymmetry in Xi0 -> Lambda gamma. The branching fraction of the decay has been measured to be Br(Xi0 -> Lambda gamma) = (1.16 +- 0.05_stat +- 0.06_syst) x 10^-3.Comment: 15 pages, 5 figures. Accepted for publication in Phys. Lett.

Electrically excitable normal rat kidney fibroblasts: A new model system for cell-semiconductor hybrids.

In testing various designs of cell-semiconductor hybrids, the choice of a suitable type of electrically excitable cell is crucial. Here normal rat kidney (NRK) fibroblasts are presented as a cell line, easily maintained in culture, that may substitute for heart or nerve cells in many experiments. Like heart muscle cells, NRK fibroblasts form electrically coupled confluent cell layers, in which propagating action potentials are spontaneously generated. These, however, are not associated with mechanical disturbances. Here we compare heart muscle cells and NRK fibroblasts with respect to action potential waveform, morphology, and substrate adhesion profile, using the whole-cell variant of the patch-clamp technique, atomic force microscopy (AFM), and reflection interference contrast microscopy (RICM), respectively. Our results clearly demonstrate that NRK fibroblasts should provide a highly suitable test system for investigating the signal transfer between electrically excitable cells and extracellular detectors, available at a minimum cost and effort for the experimenters

MYSM1 maintains ribosomal protein gene expression in hematopoietic stem cells to prevent hematopoietic dysfunction.

Ribosomopathies are congenital disorders caused by mutations in the genes encoding ribosomal and other functionally related proteins. They are characterized by anemia, other hematopoietic and developmental abnormalities, and p53 activation. Ribosome assembly requires coordinated expression of many ribosomal protein (RP) genes; however, the regulation of RP gene expression, especially in hematopoietic stem cells (HSCs), remains poorly understood. MYSM1 is a transcriptional regulator essential for HSC function and hematopoiesis. We established that HSC dysfunction in Mysm1 deficiency is driven by p53; however, the mechanisms of p53 activation remained unclear. Here, we describe the transcriptome of Mysm1-deficient mouse HSCs and identify MYSM1 genome-wide DNA binding sites. We establish a direct role for MYSM1 in RP gene expression and show a reduction in protein synthesis in Mysm1(-/-) HSCs. Loss of p53 in mice fully rescues Mysm1(-/-) anemia phenotype but not RP gene expression, indicating that RP gene dysregulation is a direct outcome of Mysm1 deficiency and an upstream mediator of Mysm1-/phenotypes through p53 activation. We characterize a patient with a homozygous nonsense MYSM1 gene variant, and we demonstrate reduced protein synthesis and increased p53 levels in patient hematopoietic cells. Our work provides insights into the specialized mechanisms regulating RP gene expression in HSCs and establishes a common etiology of MYSM1 deficiency and ribosomopathy syndromes