Einfluß von Lipidfraktionen mikrobieller Herkunft auf die Wasserausnutzung in der biologissechen Stoffproduktion von Kulturpflanzen

Effects of exogenous applied lipids being of microbial origin on the water use efficiency (WUE) and the biomass production have been studied in pot and field experiments using crop plants. Lipid mixtures extracted from the cells of Candida maltosa EH 15 increased the WUE (9…16%) and the grain yield (÷x = 10%) of the wheat and barley plants under dry conditions. The fatty acid fraction separated from the lipid mixtures also improved the WUE especially under stress (20…100%) and the biomass production. The phosphatide fraction emulsified with sulfonate containing solvents was not physiologically active.     

Die Entwicklungsfähigkeiten isolierter Furchungszellen aus dem Ei des KaninchensOryctolagus cuniculus

Ohne Zusammenfassung Otto Koehler am 20. 12. 1959 zu seinem 70. Geburtstag.     

Suppression of GLUT1; A new strategy to prevent diabetic complications

High blood glucose results in high glucose levels in retina, because GLUT1, the sole glucose transporter between blood and retina, transports more glucose when blood glucose is high. This is the ultimate cause of diabetic retinopathy. Knockdown of GLUT1 by intraocular injections of a pool of siRNAs directed against SLC2A1 mRNA which codes for GLUT1 significantly reduced mean retinal glucose levels in diabetic mice. Systemic treatment of diabetic mice with forskolin or genistein, which bind GLUT1 and inhibit glucose transport, significantly reduced retinal glucose to the same levels seen in non‐diabetics. 1,9‐Dideoxyforskolin, which binds GLUT1 but does not stimulate adenylate cyclase had an equivalent effect to that of forskolin regarding lowering retinal glucose in diabetics indicating that cyclic AMP is noncontributory. GLUT1 inhibitors also reduced glucose and glycohemoglobin levels in red blood cells providing a peripheral biomarker for the effect. In contrast, brain glucose levels were not increased in diabetics and not reduced by forskolin. Treatment of diabetics with forskolin prevented early biomarkers of diabetic retinopathy, including elevation of superoxide radicals, increased expression of the chaperone protein β2 crystallin, and increased expression of vascular endothelial growth factor (VEGF). These data identify GLUT1 as a promising therapeutic target for prevention of diabetic retinopathy. J. Cell. Physiol. 228: 251–257, 2013. © 2012 Wiley Periodicals, Inc.     

Zell- und stoffwechselphysiologische Untersuchungen an der Wurzel von Lemna minor L. unter besonderer Berücksichtigung von Kalium- und Kalziummangel

Ohne ZusammenfassungMit 12 Textabbildungen.Im Auszug vorgetragen auf der Botanikertagung Kassel 1949.     

Receptor Binding Sites and Antigenic Epitopes on the Fiber Knob of Human Adenovirus Serotype 3

The adenovirus fiber knob causes the first step in the interaction of adenovirus with cell membrane receptors. To obtain information on the receptor binding site(s), the interaction of labeled cell membrane proteins to synthetic peptides covering the adenovirus type 3 (Ad3) fiber knob was studied. Peptide P6 (amino acids [aa] 187 to 200), to a lesser extent P14 (aa 281 to 294), and probably P11 (aa 244 to 256) interacted specifically with cell membrane proteins, indicating that these peptides present cell receptor binding sites. Peptides P6, P11, and P14 span the D, G, and I β-strands of the R-sheet, respectively. The other reactive peptides, P2 (aa 142 to 156), P3 (aa 153 to 167), and P16 (aa 300 to 319), probably do not present real receptor binding sites. The binding to these six peptides was inhibited by Ad3 virion and was independent of divalent cations. We have also screened the antigenic epitopes on the knob with recombinant Ad3 fiber, recombinant Ad3 fiber knob, and Ad3 virion-specific antisera by enzyme-linked immunosorbent assay. The main antigenic epitopes were presented by P3, P6, P12 (aa 254 to 269), P14, and especially the C-terminal P16. Peptides P14 and P16 of the Ad3 fiber knob were able to inhibit Ad3 infection of cells.