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Titlebook: Liver Diseases in Infancy and Childhood; Samuel R. Berenberg Book 1976 Martinus Nijhoff Medical Division - The Hague 1976 childhood.fetus.

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樓主: Iridescent
41#
發(fā)表于 2025-3-28 15:24:58 | 只看該作者
Bile Acid Sulfation and Cholestasis,patic parenchymal cell, the biliary ducts or both. Regardless of the etiology or the site of the lesion, cholestasis produces profound alterations in bile acid metabolism with elevated concentrations of these compounds in peripheral blood and tissues.
42#
發(fā)表于 2025-3-28 19:29:43 | 只看該作者
43#
發(fā)表于 2025-3-28 23:22:50 | 只看該作者
44#
發(fā)表于 2025-3-29 05:41:38 | 只看該作者
Neonatal Susceptibility to MHV3 Infection in Mice,r example, several viral infections — e.g. herpes virus — lead to the development of severe disease contrasting with the benign form presented by normal adults. In addition, for reasons which are still unknown, newborns often developed persistent viral infections. In mice, it has been shown that age
45#
發(fā)表于 2025-3-29 11:05:52 | 只看該作者
Portal Hypertension in Early Childhood: Etiology and Diagnostic Procedures,e space limitations exclude any discussion of children with portal hypertension resulting from primary hepatic disease. It seems appropriate to limit the discussion in this manner since other sections of this book are concerned with the surgical aspects of portal hypertension and most of the surgica
46#
發(fā)表于 2025-3-29 12:56:03 | 只看該作者
47#
發(fā)表于 2025-3-29 16:59:51 | 只看該作者
48#
發(fā)表于 2025-3-29 20:45:02 | 只看該作者
Pathologic Liver Changes in Alpha-1-Antitrypsin Deficient Infants (Pi ZZ Phenotype),Since the first report of Freier, Sharp and Bridge in 1968, many authors have stressed the association of alpha-1-antitrypsin deficiency and liver disease in children. Aagenaes, in 1972, was the first to emphasize the frequency of prolonged neonatal cholestasis.
49#
發(fā)表于 2025-3-30 00:01:31 | 只看該作者
50#
發(fā)表于 2025-3-30 07:04:30 | 只看該作者
Liver Replacement in Children,In the 10?years between the spring of 1963 and the fall of 1974, liver transplantation was attempted in 93 patients by removing the diseased native liver and replacing it with a cadaveric homograft in the natural (orthotopic) location. Fifty-six of the liver recipients were 18 years old or younger; the other 37 were adults.
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