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David A. Shafritz
Researcher at Albert Einstein College of Medicine
Publications - 8
Citations - 543
David A. Shafritz is an academic researcher from Albert Einstein College of Medicine. The author has contributed to research in topics: Hepatitis B virus DNA polymerase & Albumin. The author has an hindex of 7, co-authored 8 publications receiving 532 citations. Previous affiliations of David A. Shafritz include University of the Witwatersrand.
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Identification of integrated hepatitis B virus DNA sequences in human hepatocellular carcinomas
TL;DR: DNA extracts from hepatocellular carcinomas of 13 patients from South Africa suggest that integration of HBV‐DNA into the human genome occurs in conjunction with malignant transformation.
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Role of thyroid hormone in stimulating liver repopulation in the rat by transplanted hepatocytes
R. Oren,Mariana D. Dabeva,Anthony N. Karnezis,Anthony N. Karnezis,Petko M. Petkov,Richard Rosencrantz,Jaswinder Sandhu,Steven F. Moss,S Wang,Ethel Hurston,Ezio Laconi,Peter R. Holt,Swan N. Thung,Liang Zhu,Liang Zhu,David A. Shafritz +15 more
TL;DR: Thyroid hormone can replace PH in the RS‐based rat liver repopulation model and therefore represents a significant advance in developing methods for hepatocyte transplantation.
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Liver disease activity and hepatitis B virus replication in chronic delta antigen-positive hepatitis B virus carriers
TL;DR: It is suggested that liver disease activity in delta antigen‐positive/HBsAg‐positive carriers is more related to persistent delta infection than to continued hepatitis B virus replication, whereas production of delta components continues at high levels.
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Restoration of serum albumin levels in nagase analbuminemic rats by hepatocyte transplantation
TL;DR: The ability of this protocol for hepatocyte transplantation to restore a major biosynthetic and physiological function of the liver is demonstrated, and its potential use as a method to treat genetic‐based or acquired liver diseases is suggested.
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Changes in albumin, α-fetoprotein and collagen gene transcription in CCl4-induced hepatic fibrosis
TL;DR: It is suggested that a switch from albumin to α‐fetoprotein gene transcription can serve as a marker of liver regenerative capacity, and that this process is altered during and after development of hepatic fibrosis.