Mannich-Basen von Hydroxy-indolen, 2. Mitt

Mannich Bases of Hydroxyindoles, II¹ The 2-hydroxy-cyclohept[b]indolones 2a-c react with bis(dimethylamino)methane to yield the phenol Mannich bases 3a-c . The 1,3-benzoxazine derivatives 5a-c are synthesized from 2a,b,d and hexahydrotriethyl-1,3,5-triazine 4 . Reaction of 6-hydroxyindole 6 with triazine 4 yields benzoxazine 7 .     

Prostaglandin E2 inhibits its own renal transport by downregulation of organic anion transporters rOAT1 and rOAT3

Prostaglandin E2 (PGE2) is the principal mediator of fever and inflammation. Recently, evidence emerged that during febrile response, PGE2 that is generated in the periphery enters the hypothalamus and contributes to the maintenance of fever. In a rat model of fever generation, peripheral PGE2 is increased, whereas clearance by metabolism of peripheral PGE2 is downregulated. The major route of PGE2 excretion is via the renal proximal tubular organic anion secretory system, where basolateral uptake that is mediated by renal organic anion transporter 1 (rOAT1) and rOAT3 is rate limiting. Therefore, it was hypothesized that PGE2 itself will abolish its excretion by rOAT1 or rOAT3. Fluorescein was used as a prototypic organic anion, and NRK-52E cells from rat served as a proximal tubular model system. PGE2 time-dependently downregulates basolateral organic anion uptake, without affecting cell volume or cell protein, recirculation of counter ions, or proximal tubular transport systems in general. In addition, PGE2 diminishes expression of both rOAT1 and rOAT3. Both organic anion uptake and expression of rOAT1 and rOAT3 are dose-dependently downregulated by PGE2. These findings suggest that during fever or inflammation, renal secretory transport of PGE2 is reduced, contributing to elevated PGE2 levels in blood. These data fit into the hypothetical concept of peripheral PGE2's playing a significant role in fever. The described regulatory mechanism may also be of relevance in chronic inflammatory events. Moreover, the data presented could explain why increased plasma urate levels occur in diseases that go along with increased levels of PGE2.     

Die kolloidalen Änderungen der Muskelstrukturen und die Änderungen der Lichtstreuung durch den Muskel

Ohne ZusammenfassungMit 10 TextabbildungenMit Unterstützung des Schweizerischen Nationalfonds.     

Propionyl-CoA carboxylase deficiency with overflow of metabolites of isoleucine catabolism at all levels

An 11-year old girl with spastic paraplegia and mental retardation has suffered from attacks of metabolic acidosis since the age of 18 months. Ketotic hyperglycinemia was diagnosed when she was 3 years old. Reinvestigation at 9 1/2 years included a two-day load with L-isoleucine, and propionyl-CoA carboxylase assay in cultured fibroblasts. The following compounds increased following the load: 3-hydroxypropionic acid, 2-methyl-3-hydroxybutyric acid, 2-ethylhydracrylic acid, 3-hydroxy-n-valeric acid, 3-oxo-n-valeric acid, 2-methyl-3-oxobutyric acid, 2-oxo-3-methylvaleric acid, 2-methyl-3-oxovaleric acid, N-tiglylglycine, methylcitric acid and butanone. Small amounts of alloisoleucine appeared in plasma. Propionyl-CoA carboxylase deficiency was suggested by this metabolite pattern and demonstrated in cultured fibroblasts.With support of the Landesamt für Wissenschaft und Forschung des Landes Nordrhein-WestfalenWith support of Het Praeventiefonds     

Demonstration von fetalem Hämoglobin in den Erythrocyten eines Blutausstrichs

Ohne Zusammenfassung