Publications by authors named "R Bergfeld"

Three of the major biochemical pathways implicated in the pathogenesis of hyperglycemia induced vascular damage (the hexosamine pathway, the advanced glycation end product (AGE) formation pathway and the diacylglycerol (DAG)-protein kinase C (PKC) pathway) are activated by increased availability of the glycolytic metabolites glyceraldehyde-3-phosphate and fructose-6-phosphate. We have discovered that the lipid-soluble thiamine derivative benfotiamine can inhibit these three pathways, as well as hyperglycemia-associated NF-kappaB activation, by activating the pentose phosphate pathway enzyme transketolase, which converts glyceraldehyde-3-phosphate and fructose-6-phosphate into pentose-5-phosphates and other sugars. In retinas of diabetic animals, benfotiamine treatment inhibited these three pathways and NF-kappaB activation by activating transketolase, and also prevented experimental diabetic retinopathy.

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The spatial and temporal expression of arabinogalactan proteins (AGPs) in the coleoptile of maize seedlings was investigated with monoclonal antibodies (MAC207, JIM13, JIM14) raised against particular AGP epitopes in carrot. MAC207 binds to a buffer-soluble AGP fraction of 90-210 kDa that also reacts with beta-glucosyl Yariv reagent and the lectin RCA120. Immunogold-labelling showed that the MAC207 epitope is exclusively localized in the plasma membrane.

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Auxin (indole-3-acetic acid) controls the orientation of cortical microtubes (MT) at the outer wall of the outer epidermis of growing maize coleoptiles (Bergfeld, R., Speth, V., Schopfer, P.

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The involvement of cell-wall polymer synthesis in auxin-mediated elongation of coleoptile segments from Zea mays L. was investigated with particular regard to the growth-limiting outer epidermis. There was no effect of indole acetic acid (IAA) on the incorporation of labeled glucose into the major polysaccharide wall fractions (cellulose, hemicellulose) within the first 2 h of IAA-induced growth.

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It was inferred from previous findings that a plastid-derived factor (plastidic factor) is involved in the transcriptional control of nuclear genes coding for proteins destined for the chloroplast. Photooxidative damage to the plastid destroys the ability of the organelle to give off this factor. Cytosolic enzyme levels are not impaired if plastids are damaged, and morphogenesis of seedlings is normal.

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