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O Haferkamp

Publications and source records attributed to O Haferkamp.

176 records · Page 10Linked to original sources
PubMedDate not supplied

[O-Methylation of epinephrine, 3,4-dihydroxybenzoic acid and 6,7-dihydroxycoumarin in yeasts (author's transl)].

In the yeasts C. albicans, C. tropicalis, and C. stellatoidea but not in C. krusei, R.rubra, and S. cerevisiae enzyme activity was found by which--as by the catechol-O-methyltransferase (EC 2.1.1.6) found in the liver--the O-methylation of epinephrine to metanephrine and paranephrine, of 3,4-dihydroxybenzoic acid to 4-hydroxy-3-methoxybenzoic acid and 3-hydroxy-4-methoxybenzoic acid, and of 6,7-dihydroxycoumarin to 7-hydroxy-6-methoxycoumarin and 6-hydroxy-7-methoxycoumarin is catalysed. When the substrates 3,4-dihydroxybenzoic acid, or 6,7-dihydroxycoumarin or epinephrine were incubated in the presence of S-adenosyl-L-[methyl-14C]methionine and S-adenosylmethionine hydrogensulfate with a 100 000 X g supernatant of C. albicans, C. tropicalis or C. stellatoidea the corresponding O-methylethers were detected in the extracts of the incubation medium by thin-layer chromatography. Final identification of the isomeric radioactive O-methylethers obtained from 3,4-dihydroxybenzoic acid and 6,7-dihydroxycoumarin was performed after thin-layer chromatographic separation by the reversed isotope dilution technique. The radioactive m- and p-O-methyl derivatives from epinephrine were separated by thin-layer chromatography and then cleaved with periodate to the corresponding aldehydes which were also identified mainly by the reversed isotope dilution technique.

Candida↗
PubMedDate not supplied

Prostaglandins and their precursors in rheumatoid arthritis: progress and problems.

Evidence is presented to support the hypothesis that prostaglandins and their precursors, collectively termed prostanoids, have an important role to play in the pathogenesis of joint destruction in arthritis, with particular reference to rheumatoid arthritis. After discussion of the role of prostanoids as mediators of inflammation, evidence is given that prostanoids are present in the joints of patients with rheumatoid arthritis, that these substances are capable of causing joint damage in vitro and in vivo, and that drugs which are able to arrest the progress of the arthritic condition or bring symptomatic relief possess the ability to inhibit prostanoid synthesis in vivo and in vitro.

Animals↗
PubMedDate not supplied

Influence of nonsteroidal anti-inflammatory agents on lapine articular chondrocyte growth in vitro.

The lapine articular chondrocyte monolayer was used to study the effects of cell proliferation, morphology, nd synthesis of proteoglycans of four nonsteroidal anti-inflammatory agents piroxicam, diclofenac sodium, sulindac sulfiphe, and indomethacin. None of the substances caused any alteration to chondrocyte morphology. Cell proliferation and macromolecular binding of 35SO4 were unaffected by piroxicam (0.2, 2, and 20 micrograms/ml) or diclofenac sodium (0.2, 2, and 5 micrograms/ml). Whereas indomethacin markedly reduced cell proliferation (100 mumol/l; p less than 0.01), it failed to alter net proteoglycan synthesis significantly (1, 10, and 100 mumol/l). Sulindac sulfiphe significantly reduced chondrocyte proliferation at 0.5 and 5 micrograms/ml (p less than 0.01). The 0.5 micrograms/ml concentration also markedly stimulated proteoglycan synthesis (171%; p less than 0.01). The use of the articular chondrocyte monolayer as an experimental model to investigate drug-induced alterations of cartilage metabolism is discussed.

Animals↗
PubMedDate not supplied

Disseminated neocortical and subcortical encephalopathy (DNSE) with widespread activation of brain macrophages: a new dementia disorder? Autopsy reports of two postmenopausal women from families with mitochondrial DNA mutations.

In this study we present 2 postmenopausal women who showed clinical symptoms that resembled those of a rather well-defined group of vascular dementia disorders, termed subcortical dementia (Binswanger disease, CADASIL). Patient 1 exhibited mitochondrial DNA (mtDNA) variants in the ND5 gene at position 13,708 and the Cytb gene at position 15,257. These DNA variants have been described in a number of neurologic disorders, but their pathogenetic potential is unclear. Patient 2 showed the same DNA alterations and an additional mtDNA variant at position 15,812 in the Cytb gene. The principal neurohistologic features of the 2 atrophic brains presented here include: subtotal selective neuronal cell loss in the cortex and, to a lesser degree, in the basal ganglia (claustrum, putamen, globus pallidus), sparing palaeocortex and periarchaeocortex, and a very characteristic and diagnostic feature was detachment of astrocytic processes from capillary walls resulting in pericapillary space formation. These pericapillary spaces were partially filled with macrophages. The spaces were not associated with total breakdown of the blood vessel walls as demonstrated by the absence of erythrocytes, lymphocytes, or polymorphonuclear leukocytes outside the vascular bed of the brain; progressive subcortical encephalopathy, as it is seen in subcortical dementia (Binswanger), but lacking arterial lipohyalinosis. The cerebral grey and white matter revealed cuffing of arteries and arterioles by adventitial macrophages. The neocortical and subcortical changes were accompanied by myriads of activated macrophages filled with lipids. The pathology of our 2 cases differs from that of other neurodegenerative disorders and we suggest the term of "disseminated neocortical and subcortical encephalopathy (DNSE) with widespread activation of brain macrophages".

Basal Ganglia↗