Countries citing papers authored by Sheldon M. Epstein
Since
Specialization
Citations
This map shows the geographic impact of Sheldon M. Epstein's research. It shows the number of citations coming from papers published by authors working in each country. You can also color the map by specialization and compare the number of citations received by Sheldon M. Epstein with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Sheldon M. Epstein more than expected).
Fields of papers citing papers by Sheldon M. Epstein
This network shows the impact of papers produced by Sheldon M. Epstein. Nodes represent research fields, and links connect fields that are likely to share authors. Colored nodes show fields that tend to cite the papers produced by Sheldon M. Epstein. The network helps show where Sheldon M. Epstein may publish in the future.
Co-authorship network of co-authors of Sheldon M. Epstein
This figure shows the co-authorship network connecting the top 25 collaborators of Sheldon M. Epstein.
A scholar is included among the top collaborators of Sheldon M. Epstein based on the total number of
citations received by their joint publications. Widths of edges
represent the number of papers authors have co-authored together.
Node borders
signify the number of papers an author published with Sheldon M. Epstein. Sheldon M. Epstein is excluded from
the visualization to improve readability, since they are connected to all nodes in the network.
Epstein, Sheldon M., et al.. (1982). Cyclic nucleotide modulation of in vitro morphological transformation of Syrian hamster cells.. PubMed. 42(4). 1274–8.4 indexed citations
3.
Epstein, Sheldon M., et al.. (1980). Relationship between morphological transformation and [3H]thymidine incorporation stimulated by a chemical carcinogen in postconfluent cultures of hamster embryo cells.. PubMed. 40(7). 2411–6.3 indexed citations
Merkow, Leonard P., Sheldon M. Epstein, Malcolm Slifkin, & Matias Pardo. (1973). The ultrastructure of renal neoplasms induced by aflatoxin B1.. PubMed. 33(7). 1608–14.14 indexed citations
6.
Chayoth, Reuben, Sheldon M. Epstein, & James B. Field. (1973). Glucagon and prostaglandin E1 stimulation of cyclic adenosine 3', 5'-monophosphate levels and adenylate cyclase activity in benign hyperplastic nodules and malignant hepatomas of ethionine-treated rats.. PubMed. 33(8). 1970–4.36 indexed citations
Witschi, Hanspeter, Sheldon M. Epstein, & Emmanuel Farber. (1971). Influence of liver regeneration on the loss of fluorenylacetamide derivative bound to liver DNA.. PubMed. 31(3). 270–3.12 indexed citations
9.
Merkow, Leonard P., Sheldon M. Epstein, Herschel Sidransky, Ethel Verney, & Matias Pardo. (1971). The pathogenesis of experimental pulmonary aspergillosis. An ultrastructural study of alveolar macrophages after phagocytosis of a flavus spores in vivo.. PubMed. 62(1). 57–74.62 indexed citations
Epstein, Sheldon M., et al.. (1969). Renal epithelial neoplasms induced in male Wistar rats by oral aflatoxin B1.. PubMed. 29(5). 1045–50.38 indexed citations
Epstein, Sheldon M., Thomas D. Miale, John Moossy, Ethel Verney, & Herschel Sidransky. (1968). EXPERIMENTAL INTRACRANIAL ASPERGILLOSIS. Journal of Neuropathology & Experimental Neurology. 27(3). 473–482.10 indexed citations
Epstein, Sheldon M., Nobuyuki Ito, Leonard P. Merkow, & Emmanuel Farber. (1967). Cellular analysis of liver carcinogenesis: the induction of large hyperplastic nodules in the liver with 2-fluorenylacetamide or ethionine and some aspects of their morphology and glycogen metabolism.. PubMed. 27(9). 1702–11.169 indexed citations
18.
Epstein, Sheldon M., E. Verney, Thomas D. Miale, & Herschel Sidransky. (1967). Studies on the pathogenesis of experimental pulmonary aspergillosis.. PubMed. 51(5). 769–88.48 indexed citations
19.
Epstein, Sheldon M., et al.. (1965). Pyridine nucleotides in the thyroid. Biochimica et Biophysica Acta (BBA) - General Subjects. 100(1). 13–27.6 indexed citations
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Rankless may not fully capture the entirety of a scholar's output or impact.