Coupling of the antiviral drug ara‐AMP to lactosaminated albumin leads to specific uptake in rat and human hepatocytes

Robert W. Jansen, Johan K. Kruijt, THEO J. C. van Berkel, Dirk K. F. Meije – 1 July 1993 – We covalently coupled 9‐β‐D‐arabinofuranosyladenine 5′‐monophosphate (ara‐AMP) to the carrier molecule lactosaminated human serum albumin using a water‐soluble carbodiimide with a two‐step conjugation method (pH 4.5 and pH 7.5) instead of the commonly used single‐step conjugation at pH 7.5. This resulted in a predominantly monomeric conjugate (lac27‐HSA–ara‐AMP9). The conjugate was stable in buffer (pH 7.4) and blood plasma.

Effects of ethanol on prostanoid production by liver fat‐storing cells

Robert Flisiak, Enrique Baraona, Jianjun Li, Charles S. Lieber – 1 July 1993 – Fat‐storing cells participate in the development of alcoholic liver disease. To study possible effects of ethanol on prostaglandin metabolism by fat‐storing cells, we isolated them from normal rat liver. Cultured fat‐storing cells produced substantial amounts (DNA, about 2 ng/μg every 24 hr) of prostaglandin E2 and prostaglandin I2 (measured as 6‐keto prostaglandin F1α) but no significant amounts of prostaglandin F2α.

A comparison of the effects of aflatoxin B1 on the livers of rats and duck hepatitis B virus–infected and noninfected ducks

Alan A. Seawright, Roger T. Snowden, I. Olusola Olubuyide, Joan Riley, David J. Judah, Gordon E. Neal – 1 July 1993 – A need exists for an appropriate animal model for the involvement of both hepatitis B virus infection and ingestion of aflatoxins in the etiology of liver cancer. Duck hepatitis B virus–infected ducks, on the basis of hepatoma development in the wild in China, appear to offer this possibility. The duck has been reexamined as a model system, and key metabolic processes have been assayed in comparison with the rat model for hepatocarcinogenesis.

Restructuring American health care financing: First of all, do no harm!

Paul D. Berk – 1 July 1993 – Health care costs are climbing throughout the western world. Aging populations and the costs of advanced technology are the principal forces behind much of this global increase. No country has yet succeeded in containing these growing costs other than by some form of rationing. A variety of experimental strategies, including managed competition, are being considered or tested, but none is clearly effective.

Reestablishment of cell polarity of rat hepatocytes in primary culture

Alexandru I. Musat, Carol A. Sattler, Gerald L. Sattler, Henry C. Pitot – 1 July 1993 – The cell–basement membrane interaction is an important determinant of epithelial cell polarity. Although hepatocytes in situ are polarized, no morphologically identifiable basement membrane is found at their basal surface. However, several studies have demonstrated immunoreactivity to basement membrane proteins in the space of Disse, indicating the existence of an extracellular matrix, albeit of low density.

Tissue eicosanoids and vascular permeability in rats with chronic biliary obstruction

Narumi Ohara, Norbert F. Voelke, Shih‐Wen Chang – 1 July 1993 – Advanced cirrhosis is known to be associated with extrahepatic organ dysfunction, but the mechanism for this cirrhosis complication is largely unknown. We measured tissue albumin leakage in rats with biliary cirrhosis or acute cholestasis and tested the hypothesis that arachidonic acid metabolites contribute to the vascular permeability change.

Hyperglycemia reduces gallbladder emptying and plasma hormone secretion to modified sham feeding and regular feeding

Sybrand Y. de Boer, Ad A. M. Masclee, Wai Fan Lam, Jaap Schipper, Jan B. M. J. Jansen, Cornelius B. H. W. Lamers – 1 June 1993 – The purpose of this study was to investigate the effect of acute stable hyperglycemia on gallbladder motility, plasma cholecystokinin level and pancreatic polypeptide secretion. Gallbladder emptying in response to modified sham feeding and regular feeding was determined in six healthy subjects on two separate occasions during normoglycemia (serum glucose = 5 mmol/L) and during hyperglycemia (serum glucose = 15 mmol/L).

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