Excess HBcAg in HBc antibody–negative chronic hepatitis B virus carriers

Yamina Lazizi, Pascal Dubreuil, Jacques Pillot – 1 June 1993 – HBcAg and antibody to HBcAg were assayed in chronic hepatitis B virus carriers who were not reactive for HBc antibodies on available commercial tests. HBc antibody–negative sera, collected before the onset of the acute phase in recovering patients, were used as controls. A high level of HBcAg was detected in HBc antibody–negative chronic hepatitis B virus carriers after dissociative treatment. HBcAg levels were correlated with serum hepatitis B virus DNA levels.

Passage of amino acids and glucose across the blood‐brain barrier in patients with hepatic encephalopathy

Gitte M. Knudsen, Jes Schmidt, Thomas Almdal, Olaf B. Paulson, Hendrik Vilstrup – 1 June 1993 – We repeatedly measured blood‐brain barrier passage of phenylalanine, leucine, glucose and GABA in nine patients with hepatic encephalopathy using the intravenous double‐indicator technique. Controls were four patients without liver disease and two of the patients who had recovered completely from their hepatic encephalopathy. The corrected cerebral venous output curves were fitted by use of a three‐compartment model with four parameters.

A macroregenerative nodule containing multiple foci of hepatocellular carcinoma in a noncirrhotic liver

Neil D. Theise, Jonathan D. Lapook, Swan N. Thung – 1 June 1993 – We report an incidental small hepatocellular carcinoma in a patient with chronic hepatitis C infection without cirrhosis. The existence of portal triads and the Meyenburg complexes within the lesion and atypical subnodules suggests that the carcinoma has arisen in the context of a macroregenerative nodule rather than the whole nodule being an early, spreading carcinoma. A growing body of evidence supports macroregenerative nodules as being precursor lesions in the development of hepatocellular carcinoma.

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).

Expression of the terminal protein of hepatitis B virus is associated with failure to respond to interferon therapy

Graham R. Foster, Robert D. Goldin, Andrew Hay, Michael J. McGarvey, George R. Stark, Howard C. Thomas – 1 May 1993 – The terminal protein domain of the hepatitis B viral polymerase can inhibit the cellular response to interferon. To clarify the clinical relevance of this inhibitory effect, we examined the expression of terminal protein in liver biopsy specimens from patients with chronic hepatitis B infection.

Monoclonal antibody against the CD18 adhesion molecule stimulates glucose uptake by the liver and hepatic nonparenchymal cells

Abraham P. Bautista, Zoltan Spolarics, Hartmut Jaeschke, C. Wayne Smith, John J. Spitzer – 1 May 1993 – Neutrophils and macrophages play an important role in the body's microbicidal defense and have been implicated in the induction of tissue injury in reperfusion, endotoxemia and septic shock. Cellular host defense is accompanied by enhanced glucose use. In this study we examined the effect of monoclonal antibody 1F12 on in vivo glucose use by selected tissues and hepatic phagocytes.

Drug targeting to the liver with bile acids: THE “trojan horse” resurrected?

Dirk K. F. Meijer – 1 May 1993 – Bile acids are selectively taken up from portal blood into the liver by specific transport systems in the hepatocyte plasma membrane. Therefore, studies were performed to evaluate the potential of bile acids as shuttles to deliver drugs specifically to the liver. The alkylating cytostatic drug chlorambucii and the fluorescent prolyl‐4‐hydroxylase inhibitor 4‐nitrobenzo‐2‐oxa‐1,3‐diazol‐β‐Ala‐Phe‐5‐oxaproline‐Gly were covalently linked via an amide bond to 7α, 12α,‐dihydroxy‐3β‐(ω‐aminoalkoxy)‐5‐β‐cholan‐24‐oic acid.

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