Baruch S. Blumberg

Bio: Baruch S. Blumberg is an academic researcher from Fox Chase Cancer Center. The author has contributed to research in topics: Hepatitis B virus & Hepatitis B. The author has an hindex of 45, co-authored 156 publications receiving 9395 citations. Previous affiliations of Baruch S. Blumberg include Ames Research Center & University of Oxford.

A New Antigen in Leukemia Sera

Abstract: Patients who receive large numbers of transfusions for anemia and other causes may develop precipitins in their blood. These precipitins may react in agar gel double diffusion experiments with specific human serum lipoprotein found in the blood of other individuals. Since these precipitins were found only in patients who had received transfusions they were thought to be antibodies against serum lipoproteins which developed in the patients as a result of the repeated transfusions. The precipitin is referred to as an isoprecipitin since it develops against a specificity found in an individual from the same species. The antilipoprotein isoprecipitin1,2developed in approximately 30% of 47 patients with thalassemia who had received transfusions. Isoprecipitins also developed in smaller number of transfused patients with other diseases. All precipitins stained with sudan black, a dye specific for lipid. Immunoelectrophoretic and ultracentrifugal studies showed that the protein with which the isoprecipitins reacted was a

A serum antigen (Australia antigen) in Down's syndrome, leukemia, and hepatitis.

Abstract: Excerpt We have previously reported the presence of an isoantigen of human sera, rare or absent in normal U. S. and northern European populations but relatively common in patients with leukemia (1,...

The hepatitis C virus p7 protein forms an ion channel that is inhibited by long-alkyl-chain iminosugar derivatives

Abstract: We show that hepatitis C virus (HCV) p7 protein forms ion channels in black lipid membranes. HCV p7 ion channels are inhibited by long-alkyl-chain iminosugar derivatives, which have antiviral activity against the HCV surrogate bovine viral diarrhea virus. HCV p7 presents a potential target for antiviral therapy.

Particles associated with Australia Antigen in the Sera of Patients with Leukaemia, Down's Syndrome and Hepatitis

Abstract: AUSTRALIA antigen was first identified using an antiserum produced in a transfused patient1,2. The antiserum gave a clear precipitin line in a double diffusion experiment when placed adjacent to the serum from an Australian aborigine. Pending further identification of the antigen, the geographic name “Australian antigen” was given to the reacting material found in the aborigine's serum. Specific antisera against this antigen can be produced by immunizing rabbits with serum containing Australia antigen, and subsequent absorption with serum which does not contain Australia antigen3. The precipitin band which forms between the haemophilia antiserum and the serum containing Australia antigen stains faintly with sudan black, indicating that the antigen contains lipid. It has a specific gravity of less than 1.21 and appears in the first peak in ‘Sephadex G-200’ column chromatography (indicating a high molecular weight)4.

Use of targeted glycoproteomics to identify serum glycoproteins that correlate with liver cancer in woodchucks and humans.

Abstract: Chronic infection with hepatitis B virus (HBV) is associated with the majority of hepatocellular carcinoma (HCC). The diagnosis of HCC is usually made in the late stages of the disease, when treatment options are limited and prognosis is poor. We therefore have developed a method of glycoproteomic analysis in an attempt to discover serum markers that can assist in the early detection of HBV-induced liver cancer. Briefly, a comparative method for analysis of oligosaccharides released from serum glycoproteins and for recovery and identification of proteins with aberrant glycosylation, as a function of cancer diagnosis, is described. The model we have used is the woodchuck (Marmota monax), which shares similarities in the glycosylation pattern associated with liver proteins in human HCC. In this report, we show that woodchucks diagnosed with HCC have dramatically higher levels of serum-associated core α-1,6-linked fucose, as compared with woodchucks without a diagnosis of HCC. The coupling of this methodology with 2D gel proteomics has permitted the identification of several glycoproteins with altered glycosylation as a function of cancer. One such glycoprotein, Golgi Protein 73 (GP73), was found to be elevated and hyperfucosylated in animals with HCC. Further, the study showed GP73 to be elevated in the serum of people with a diagnosis of HCC, providing a validation of our approach. The potential of this technology for biomarker discovery and the implications of increased levels of GP73 in liver cancer are discussed.

Structure of serum albumin.

Abstract: Publisher Summary This chapter provides an insight of the findings of past significant papers with the current knowledge of the recently determined high resolution X-ray structure of serum albumin. The most outstanding property of albumin is its ability to bind reversibly an incredible variety of ligands. The sequences of all albumins are characterized by a unique arrangement of disulfide double loops that repeat as a series of triplets. Albumin belongs to a multigene family of proteins that includes α- fetoprotein (AFP) and vitamin D-binding protein (VDP), also known as G complement (Gc) protein. Although AFP is considered the fetal counterpart of albumin, its binding properties are distinct and it is suggested that AFP may have a higher affinity for some unknown ligands important for fetal development. Domain structure and the arrangement of the disulfides, the surface charge distribution, and the conformational flexibility of the albumin molecule are described. The nature of ligand binding, including small organics, long-chain fatty acids, and metals, to multiple sites on the albumin molecule is clearly depicted. The chapter concludes with the perceptive comments on future directions being taken to explore the structure and function of this fascinating protein.

Rising incidence of hepatocellular carcinoma in the United States.

Abstract: Background and Methods Clinical observations have suggested that the number of cases of hepatocellular carcinoma has increased in the United States. We analyzed data from the Surveillance, Epidemiology, and End Results (SEER) data base to determine the age-adjusted incidence of hepatocellular carcinoma from 1976 to 1995, data from the U.S. vital-statistics data base to determine age-adjusted mortality rates from 1981 to 1995, and data from the Department of Veterans Affairs to determine age-adjusted rates of hospitalization for the disease from 1983 to 1997. Results The incidence of histologically proved hepatocellular carcinoma increased from 1.4 per 100,000 population (95 percent confidence interval, 1.3 to 1.4) for the period from 1976 to 1980 to 2.4 per 100,000 (95 percent confidence interval, 2.3 to 2.4) for the period from 1991 to 1995. Among black men, the incidence was 6.1 per 100,000 for the period from 1991 to 1995, and among white men, it was 2.8 per 100,000. There was a 41 percent increase in ...

Hepatitis B virus infection.

Abstract: The hepatitis B virus (HBV), discovered in 1966, infects more than 350 million people worldwide.1 Hepatitis B is a leading cause of chronic hepatitis, cirrhosis, and hepatocellular carcinoma, accounting for 1 million deaths annually. Knowledge of the intricacies of viral infection and of the molecular biology of this fascinating virus has led to the successful development of a vaccine and to treatment sometimes capable of eradicating chronic infection. This review addresses many aspects of HBV infection, including the role of the immune system in determining the outcome of clinical infection, recent developments in molecular studies of the virus, and new . . .

Hepatitis B Virus Infection — Natural History and Clinical Consequences

Abstract: This review article examines the structure and replication cycle of hepatitis B virus and discusses the natural history of primary infection, the mechanisms of clearance of the virus, and reasons for persistent infection. It concludes with a discussion of what we know about the virus and how it causes hepatitis and the implications for treatment.