Rutherford Scattering at Textor - Measurements on the Ion Velocity Distribution

The Rutherford-scattering diagnostic at TEXTOR is primarily used for temporally and spatially resolved measurements of the ion temperature. Both central temperatures and temperature profiles have been measured. In addition, toroidal rotation speeds of the hydrogenic bulk ions around 10(5) ms(-1) have been found. A narrow peak in the velocity distribution of scattered particles, observed during additional heating and formerly attributed to scattering on high-Z impurities in the plasma, is now thought to be due to some parasitic process by which ionized beam particles are drifting into the line-of-sight of the analyzer

1st Measurements of the Toroidal Rotation of the Bulk Ions at Textor by Rutherford Scattering

The Rutherford scattering diagnostic at TEXTOR was used to determine the central toroidal rotation speed of the hydrogenic bulk ions in the plasma. During neutral beam injection speeds of the order of 10(5) ms-1 were found. With balanced injection no rotation was observed. A first comparison with charge exchange recombination spectroscopy showed, within the accuracy of the methods, no difference in the derived speeds, in agreement with neoclassical theory. The momentum confinement time of the central hydrogenic ions was found to decrease with the neutral beam power as approximately 1/square-root P(NBI)

Rutherford Scattering at Textor

The Rutherford scattering diagnostic at TEXTOR is used to perform temporal and spatial resolved measurements of the ion temperature. Function parametrization techniques are used for fast analysis of the complex spectra, which also contain information about the presence of impurities in the scattering volume. The (perpendicular) central ion temperature has been determined for a series of discharges, where neutral beam coinjection (hydrogen) was applied to plasmas of different densities. A temperature of 2.8 keV was found for a line-averaged electron density of 1.5 X 10(19) m-3, decreasing monotonically for higher densities to 0.8 keV at 6.0 X 10(19) m-3. When deuterium was used as heating beam species, scattering on a high-Z impurity, probably tungsten from the filaments of the NBI sources, gave a dominant contribution to the spectra

The effect of the DPP-4 inhibitor linagliptin to improve functional outcome after stroke is mediated by the CXCR4/SDF-1\u3b1 pathway.

Abstract Background and Aim: Dipeptidyl peptidase-4 (DPP-4) inhibitors (gliptins) decrease hyperglycemia by inhibiting glucagon-like peptide-1 (GLP-1)-cleavage. Gliptins can also improve stroke outcome in rodents independently from GLP-1 receptor [1,2]. However, the underlying mechanisms are unknown. We aimed to determine whether gliptins improve stroke outcome via the stromal cell-derived factor-1 \u3b1 (SDF-1\u3b1)/ Chemokine Receptor Type 4 (CXCR4) pathway, and identify additional effectors behind the efficacy. Methods: Mice were subjected to stroke by transient middle cerebral artery occlusion (MCAO). Linagliptin was administered for 3 days or 3 weeks from stroke onset. The CXCR4-antagonist AMD3100 was administered one day before MCAO until three days thereafter. Stroke outcome was assessed by measuring upper-limb function, stroke volume and neuronal survival. Brain GLP-1, GIP and SDF-1\u3b1 were quantified by ELISA. To identify additional gliptin-mediated molecular effectors, brain samples were analyzed by mass spectrometry. Results: Linagliptin specifically increased active SDF-1\u3b1 (p<0,001) but not GIP or GLP-1 brain levels. Blocking of SDF-1\u3b1/CXCR4 pathway abolished the positive effects of Linagliptin on upper-limb function and histological outcome after stroke. Moreover, Linagliptin treatment after stroke decreased the presence of peptides derived from Neurogranin and from an isoform of the Myelin basic protein. Conclusion: We showed that Linagliptin improves functional stroke outcome in a CXCR4/SDF-1\u3b1-dependent manner. Considering that Calpain activity and intracellular Ca2+ regulate Neurogranin and Myelin basic protein detection, we propose a gliptin-mediated neuroprotective mechanism via the SDF-1\u3b1/CXCR4 pathway that involves the regulation of Ca2+ homeostasis and the reduction of Calpain activity. These results provide new insights into restorative gliptin-mediated effects against stroke. References: [1] Darsalia et al., Diabetes 2013, 62(4):1289-1296. [2] Darsalia et al., Diabetes Obes Metab 2016, 18(5):537-41

The effect of DPP-4 inhibition to improve functional outcome after stroke is mediated by the CXCR4/SDF-1alpha pathway

Abstract AIM: Dipeptidyl peptidase-4 (DPP-4) inhibitors (gliptins) decrease hyperglycemia by inhibiting glucagon-like peptide-1 (GLP-1)-cleavage. Gliptins can also improve stroke outcome in rodents independently from GLP1R. However, the underlying mechanisms are unknown. We aimed to determine whether gliptins improve stroke outcome via the stromal cell-derived factor-1 \u3b1 (SDF-1\u3b1)/ Chemokine Receptor Type 4 (CXCR4) pathway, and identify additional effectors behind the efficacy. MATERIALS AND METHODS: Mice were subjected to stroke by transient middle cerebral artery occlusion (MCAO). Linagliptin was administered for 3 days or 3 weeks from stroke onset. The CXCR4-antagonist AMD3100 was administered one day before MCAO until three days thereafter. Stroke outcome was assessed by measuring upper-limb function, stroke volume and neuronal survival. Brain GLP-1, GIP and SDF-1\u3b1 were quantified by ELISA. To identify additional gliptin-mediated molecular effectors, brain samples were analyzed by mass spectrometry. RESULTS: Linagliptin specifically increased active SDF-1\u3b1 but not GIP or GLP-1 brain levels. Blocking of SDF-1\u3b1/CXCR4 pathway abolished the positive effects of Linagliptin on upper-limb function and histological outcome after stroke. Moreover, Linagliptin treatment after stroke decreased the presence of peptides derived from Neurogranin and from an isoform of the Myelin basic protein. CONCLUSIONS: We showed that Linagliptin improves functional stroke outcome in a CXCR4/SDF-1\u3b1-dependent manner. Considering that Calpain activity and intracellular Ca2+ regulate Neurogranin and Myelin basic protein detection, we propose a gliptin-mediated neuroprotective mechanism via the SDF-1\u3b1/CXCR4 pathway that involves the regulation of Ca2+ homeostasis and the reduction of Calpain activity. These results provide new insights into restorative gliptin-mediated effects against stroke