The measurement of the beta asymmetry in the decay of polarized neutrons

The beta-decay asymmetry parameter A was measured for the free neutron with high precision. A time projection chamber (TPC) and plastic scintillators were used as a track and energy detector for the decay electrons. Thus the decay volume was well defined. Electron tracks with different angle θ between the electron momentum and the neutron spin could be selected and compared with the expected cos θ distribution. A deviation from this distribution was observed and remains unexplained. Using the electron track detector only to delimit the fiducial volume and adopting the theoretically predicted cos θ distribution a value of A 0 = −0.1160±0.0015 was determined including corrections for recoil and weak magnetism. To our best knowledge this result is not influenced by the observed deviation from the cos θ distribution of the asymmetry. From this result the ratio g A g V = −1.266±0.004 can be deduced within the Standard Model. Using the recent neutron lifetime value leads to g V = 1.4172 (34) · 10 −62 J m 3 . This value is in good agreement with g V from ft (0 + →0 + ) and μ decay. (Elsevier

Supplementary Material for: A Key Role of Autophagy in Osteoblast Differentiation on Titanium-Based Dental Implants

Autophagy plays an important role in embryogenesis, for the maintenance of tissue homeostasis and the elimination of damaged subcellular structures. Furthermore, autophagy could be a mode of physiological cell death and also be implicated in cell differentiation. Thus, we hypothesized that autophagy may have an impact on the differentiation of osteoblast cells influenced by various titanium-based surfaces. Interactions between smooth, commercially available pure titanium (Ti cp), rough Ticer, acid-etched Ti cp (SS) and M1-M3 (comprised of the monoclinic phase of sodium-titanium oxides and rutile; M2 contains amorphous calcium phosphates) and human osteoblast cells were investigated. Immunofluorescent staining was used for detecting autophagy, cell cluster formation and collagen type I (Col-1) expression. Flow cytometry was employed to identify autophagy, the production of endogenous nitric oxide (NO) and the size and granularity of the cells. Rough surfaces caused osteoblast differentiation via the autophagic-dependent PI3/Akt signalling pathway. These surfaces induced the formation of discrete populations of large, granular cells, i.e. mature osteoblasts. In addition, M1-M3 provoked the development of a third population of small, granular cells, responsible for cell cluster formation, which are important for the formation of bone noduli and mineralisation. The same surfaces induced faster osteoblast maturation and enhanced NO production, a hallmark of the already mentioned processes. Neither the mature osteoblasts nor the small cells appeared after the inhibition of autophagy. Inhibition of autophagy also prevented cell cluster formation. We demonstrate that autophagy plays an essential role in the osteoblast differentiation on titanium-based surfaces with rough topography