Bestehen in der Asbildung der Artmerkmale: Unterschiede zwischen den diploiden und triploiden Bastarden von Triton palmatus und Triton alpestris ?

Volume: 55Start Page: 304End Page: 31

Xenopus amieti sp. nov. (Anura: Pipidae) from the Cameroons, another case of tetraploidy

Volume: 87Start Page: 919End Page: 92

The induction of triploidy by pressure in Xenopus laevis

Volume: 85Start Page: 20End Page: 2

Double compression oesotracheale fatale vasculaire et neurofibromateuse. [Fatal double tracheo-esophageal vascular compression and neurofibromatosis]

BACKGROUND: Vascular rings are a classical cause of tracheal and esophagus compression. We report the case of such an abnormality in an infant with neurofibromatosis. CASE REPORT: A 1 week-old male infant with a familial neurofibromatosis presented a stridor with severe respiratory distress. A vascular ring was demonstrated and operated on. The stridor persisted after surgery. A postoperative oesophagogram and tracheobronchoscopy showed an irregular compression of the oesophageal lumen, thought to be due to a residual extrinsic compression. Because the postoperative echocardiogram showed an extensive tumoral infiltration of both auricles, it was decided to not operate again the child. The postmortem examination revealed a disseminated neurofibromatosis infiltrating trachea, bronchi and also the wall of esophagus. CONCLUSION: Persisting stridor and oesotracheal compression postoperatively requires search for another cause. Association of vascular ring and neurofibromatosis is probably not fortuitous

Enzymatic conversion of bilirubin monoglucuronide to diglucuronide by rat liver plasma membranes

Formation of bilirubin monoglucuronide from unconjugated bilirubin requires a microsomal enzyme, UDP-glucuronate glucuronyltransferase (EC 2.4.1.17). Conversion of bilirubin monoglucuronide to bilirubin diglucuronide, the major bilirubin conjugate in bile, was studied in subcellular fractions of rat liver. The highest specific activity for bilirubin diglucuronide formation occurred in a fraction highly enriched in plasma membranes. Studies of reaction stoichiometry and utilization of UDP-D-[14C]glucuronic acid revealed that conversion of bilirubin monoglucuronide to bilirubin diglucuronide is not catalyzed by UDP-glucuronyltransferase, and results from transglucuronidation of bilirubin monoglucuronide, with formation of bilirubin diglucuronide and unconjugated bilirubin. When unconjugated bilirubin was infused intravenously into rats at rates exceeding the maximal hepatic excretory capacity, bilirubin monoglucuronide accumulated in serum and bilirubin diglucuronide was found exclusively in bile as the predominant bilirubin metabolite. These results suggest that formation of bilirubin diglucuronide occurs at the surface membrane of the liver cell. Conversion of bilirubin monoglucuronide to bilirubin diglucuronide may play a role in the transport of bilirubin glucuronides from liver to bil

Hepatic Conversion of Bilirubin Monoglucuronide to Diglucuronide in Uridine Diphosphate-Glucuronyl Transferase-Deficient Man and Rat by Bilirubin Glucuronoside Glucuronosyltransferase

The microsomal enzyme uridine diphosphate (UDP) glucuronate glucuronyltransferase (E.C. 2.4.1.17) catalyzes formation of bilirubin mono-glucuronide from bilirubin and UDPglucuronic acid. Bilirubin glucuronoside glucuronosyltransferase (E.C. 2.4.1.95), an enzyme concentrated in plasma membrane-enriched fractions of rat liver, converts bilirubin monoglucuronide to bilirubin diglucuronide. Bilirubin glucuronoside glucuronosyltransferase activity was studied in homogenates of liver biopsy specimens obtained from patients with the Crigler-Najjar syndrome (Type I) and in subcellular liver fractions of rats homozygous for UDP glucuronate glucuronyltransferase deficiency (Gunn strain). In patients with the Crigler-Najjar syndrome (Type I) and in Gunn rats, hepatic UDPglucuronate glucuronyltransferase activity was not measurable; however, bilirubin glucuronoside glucuronosyltransferase activity was similar to that in normal controls. The subcellular distribution of bilirubin glucuronoside glucuronosyltransferase activity in Gunn rat liver was similar to the distribution observed in normal Wistar rat liver. When bilirubin monoglucuronide was infused intravenously into Gunn rats, 29±5% of the conjugated bilirubin excreted in bile was bilirubin diglucuronide. After transplantation of normal Wistar rat kidney, which contained UDPglucuronate glucuronyltransferase activity, in Gunn rats, the serum bilirubin concentration decreased by 80% in 4 days. The major route of bilirubin removal was biliary excretion of conjugated bilirubin, approximately 70% of which was bilirubin diglucuronide. Although patients with the Crigler-Najjar syndrome (Type I) and Gunn rats lack UDP glucuronate glucuronyltransferase, their livers enzymatically convert bilirubin monoglucuronide to diglucuronide in vitro. Conversion in bilirubin monoglucuronide to diglucuronide was demonstrated in Gunn rats in vivo