Biomedical subjects

G Staudt

Publications and source records attributed to G Staudt.

At least 19 recordsLinked to original sources

PubMed2001

(22)Ne(alpha,n)(25)Mg: the key neutron source in massive stars.

The excitation function of the reaction (22)Ne(alpha,n)(25)Mg, the key neutron source in the astrophysical s process in massive stars, has been determined from threshold at E(alpha) = 570 up to 1450 keV with an experimental sensitivity of 10(-11) b. For all resonances in this energy range new resonance parameters have been measured. For a possible resonance at about 635 keV a new upper limit omega gamma < 60 neV for the strength was obtained. Based on the new data, improved reaction rates were calculated as a function of temperature. The new uncertainty limits are considerably smaller than in previous determinations, ruling out the large enhancement factors, up to 500, assumed in some stellar model calculations.

Journal Article↗

PubMed2001

12C(alpha,gamma)16O: the key reaction in stellar nucleosynthesis.

The angular distributions of gamma rays from the 12C(alpha,gamma)16O reaction have been measured at 20 energy points in the energy range E(cm) = 0.95 to 2.8 MeV. The sensitivity of the present experiment compared to previous direct investigations was raised by 1-2 orders of magnitude, by using an array of highly efficient ( 100%) Ge detectors shielded actively with BGOs, as well as high beam currents of up to 500 microA that were provided by the Stuttgart Dynamitron accelerator. The S(E1) and S(E2) factors deduced from the gamma angular distributions have been extrapolated to the range of helium burning temperatures applying the R-matrix method, which yielded S(300)(E1) = (76+/-20) keV b and S(300)(E2) = (85+/-30) keV b.

Journal Article↗

PubMed1997

Cross-talk between secretory phospholipase A2 and cytosolic phospholipase A2 in rat renal mesangial cells.

Incubation of rat glomerular mesangial cells with potent proinflammatory cytokines like interleukin 1beta, (IL- 1beta) triggers the expression of a non-pancreatic secretory phospholipase A2 (sPLA2) and increases the formation of prostaglandin E2. We show here that sPLA2 acts in an autocrine fashion on mesangial cells and induces a rapid activation of protein kinase C (PKC) isoenzymes delta and epsilon and of p42 mitogen-activated protein kinase (MAPK), two putative activators of cytosolic phospholipase A2 (cPLA2). sPLA2 also activates Raf-1 kinase in mesangial cells which integrates the signals coming from PKC for further processing along the MAPK cascade. Subsequently a phosphorylation and activation of cPLA2 is observed, thus arguing for a cross-talk between the two classes of PLA2. Pretreatment of cells with either the highly specific PKC inhibitor Ro-318220 or the highly specific MAPK kinase (MEK) inhibitor PD 98059 completely blocked the sPLA2-induced cPLA2 activation, indicating that both kinases are essential for the cross-talk between the two types of PLA2. The effect of sPLA2 is mimicked by lysophosphatidylcholine (LPC), a reaction product of sPLA2 activity. LPC stimulates PKC-epsilon, Raf-1 kinase and MAPK activation as well as cPLA2 activation with a subsequent increase in arachidonic acid release from mesangial cells. These data suggest that sPLA2 by cleaving membrane phospholipids and generating LPC and other lysophospholipids activates cPLA2 via the PKC/Raf-1/MAPK signalling pathway. Hence a network of interactions between different PLA2s is operative in mesangial cells and may contribute to the progression of glomerular inflammatory processes.

Animals↗

PubMed1996