Glenna L. Fry

2.2k total citations
34 papers, 1.9k citations indexed

About

Glenna L. Fry is a scholar working on Cardiology and Cardiovascular Medicine, Surgery and Hematology. According to data from OpenAlex, Glenna L. Fry has authored 34 papers receiving a total of 1.9k indexed citations (citations by other indexed papers that have themselves been cited), including 14 papers in Cardiology and Cardiovascular Medicine, 10 papers in Surgery and 9 papers in Hematology. Recurrent topics in Glenna L. Fry's work include Platelet Disorders and Treatments (7 papers), Antiplatelet Therapy and Cardiovascular Diseases (7 papers) and Lipid metabolism and disorders (7 papers). Glenna L. Fry is often cited by papers focused on Platelet Disorders and Treatments (7 papers), Antiplatelet Therapy and Cardiovascular Diseases (7 papers) and Lipid metabolism and disorders (7 papers). Glenna L. Fry collaborates with scholars based in United States. Glenna L. Fry's co-authors include David Chappell, J C Hoak, John C. Hoak, Dudley K. Strickland, Michelle Waknitz, Marc W. Pladet, Per‐Henrik Iverius, Arthur A. Spector, J. Bryan Smith and Richard D. Maca and has published in prestigious journals such as Nature, Science and Journal of Biological Chemistry.

In The Last Decade

Glenna L. Fry

33 papers receiving 1.8k citations

Peers — A (Enhanced Table)

Peers by citation overlap · career bar shows stage (early→late) cites · hero ref

Name h Career Trend Papers Cites
Glenna L. Fry United States 21 614 472 470 409 390 34 1.9k
Michael B. Stemerman United States 25 863 1.4× 577 1.2× 493 1.0× 245 0.6× 183 0.5× 48 2.5k
Tova Chajek‐Shaul Israel 28 723 1.2× 714 1.5× 606 1.3× 250 0.6× 781 2.0× 71 2.5k
F. Sandhofer Austria 24 580 0.9× 986 2.1× 578 1.2× 101 0.2× 876 2.2× 104 2.5k
S Ucchino Italy 16 482 0.8× 340 0.7× 340 0.7× 182 0.4× 133 0.3× 28 1.7k
Annalisa Iezzi Italy 15 326 0.5× 399 0.8× 426 0.9× 157 0.4× 296 0.8× 19 1.8k
Christiane Viedt Germany 19 567 0.9× 248 0.5× 367 0.8× 84 0.2× 317 0.8× 22 1.9k
Peter Libby United States 18 2.2k 3.6× 820 1.7× 560 1.2× 502 1.2× 396 1.0× 21 3.8k
Sadao Takahashi Japan 25 780 1.3× 639 1.4× 524 1.1× 160 0.4× 424 1.1× 60 1.9k
Repin Vs Russia 22 511 0.8× 460 1.0× 189 0.4× 80 0.2× 166 0.4× 136 1.5k
Agostino Faggiotto United States 8 288 0.5× 560 1.2× 299 0.6× 66 0.2× 153 0.4× 12 1.5k

Countries citing papers authored by Glenna L. Fry

Since Specialization
Citations

This map shows the geographic impact of Glenna L. Fry'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 Glenna L. Fry with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Glenna L. Fry more than expected).

Fields of papers citing papers by Glenna L. Fry

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Glenna L. Fry. 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 Glenna L. Fry. The network helps show where Glenna L. Fry may publish in the future.

Co-authorship network of co-authors of Glenna L. Fry

This figure shows the co-authorship network connecting the top 25 collaborators of Glenna L. Fry. A scholar is included among the top collaborators of Glenna L. Fry 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 Glenna L. Fry. Glenna L. Fry is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

20 of 20 papers shown
1.
Wilson, Katina M., Glenna L. Fry, David Chappell, Curt D. Sigmund, & Jheem D. Medh. (2001). Macrophage-Specific Expression of Human Lipoprotein Lipase Accelerates Atherosclerosis in Transgenic Apolipoprotein E Knockout Mice but Not in C57BL/6 Mice. Arteriosclerosis Thrombosis and Vascular Biology. 21(11). 1809–1815. 76 indexed citations
2.
Medh, Jheem D., et al.. (2000). Lipoprotein lipase- and hepatic triglyceride lipase-promoted very low density lipoprotein degradation proceeds via an apolipoprotein E-dependent mechanism. Journal of Lipid Research. 41(11). 1858–1871. 29 indexed citations
3.
Medh, Jheem D., et al.. (1999). Hepatic triglyceride lipase promotes low density lipoprotein receptor-mediated catabolism of very low density lipoproteins in vitro. Journal of Lipid Research. 40(7). 1263–1275. 14 indexed citations
4.
Medh, Jheem D., Glenna L. Fry, Mark E. Andracki, et al.. (1996). Lipoprotein Lipase Binds to Low Density Lipoprotein Receptors and Induces Receptor-mediated Catabolism of Very Low Density Lipoproteins. Journal of Biological Chemistry. 271(29). 17073–17080. 72 indexed citations
5.
Medh, Jheem D., et al.. (1995). The 39-kDa Receptor-associated Protein Modulates Lipoprotein Catabolism by Binding to LDL Receptors. Journal of Biological Chemistry. 270(2). 536–540. 109 indexed citations
6.
Chappell, David, Ituro Inoue, Glenna L. Fry, et al.. (1994). The Carboxy‐Terminal Domain of Lipoprotein Lipase Induces Cellular Catabolism of Normal Very Low Density Lipoproteins via the Low Density Lipoprotein Receptor—Related Protein/α2‐Macroglobulin Receptor. Annals of the New York Academy of Sciences. 737(1). 434–438. 8 indexed citations
7.
8.
9.
Chappell, David, et al.. (1993). Low density lipoprotein receptors bind and mediate cellular catabolism of normal very low density lipoproteins in vitro.. Journal of Biological Chemistry. 268(34). 25487–25493. 40 indexed citations
10.
Chappell, David, et al.. (1992). Evidence for isomerization during binding of apolipoprotein-B100 to low density lipoprotein receptors.. Journal of Biological Chemistry. 267(1). 270–279. 21 indexed citations
11.
Chappell, David, Glenna L. Fry, Michelle Waknitz, et al.. (1992). The low density lipoprotein receptor-related protein/alpha 2-macroglobulin receptor binds and mediates catabolism of bovine milk lipoprotein lipase.. Journal of Biological Chemistry. 267(36). 25764–25767. 140 indexed citations
12.
Fry, Glenna L. & John C. Hoak. (1989). [6] Measurement of platelet interaction with endothelial monolayers. Methods in enzymology on CD-ROM/Methods in enzymology. 169. 71–76. 1 indexed citations
13.
Spector, A A, et al.. (1981). Essential fatty acid availability and prostacyclin production by cultured human endothelial cells. Progress in Lipid Research. 20. 471–477. 19 indexed citations
14.
Hoak, J C, et al.. (1981). Role of the vascular endothelium. Philosophical transactions of the Royal Society of London. Series B, Biological sciences. 294(1072). 331–338. 10 indexed citations
15.
Czervionke, R L, J. Bryan Smith, Glenna L. Fry, J C Hoak, & D L Haycraft. (1979). Inhibition of prostacyclin by treatment of endothelium with aspirin. Correlation with platelet adherence.. Journal of Clinical Investigation. 63(5). 1089–1092. 78 indexed citations
16.
Maca, Richard D., et al.. (1977). The effects of intact platelets on cultured human endothelial cells. Thrombosis Research. 11(6). 715–721. 26 indexed citations
17.
Jacobsen, Carl Ditlef, et al.. (1975). Fibrinogen-fibrin related antigen pattern in human blood. Incomplete lysis of whole blood clots by Urokinase. Thrombosis Research. 6(4). 327–336.
18.
Lewis, L. J., John C. Hoak, Richard D. Maca, & Glenna L. Fry. (1973). Replication of Human Endothelial Cells in Culture. Science. 181(4098). 453–454. 113 indexed citations
19.
Spector, Arthur A., John C. Hoak, E. D. Warner, & Glenna L. Fry. (1970). Utilization of long-chain free fatty acids by human platelets. Journal of Clinical Investigation. 49(8). 1489–1496. 74 indexed citations
20.
Hoak, John C., et al.. (1969). Effects of triiodothyronine-induced hypermetabolism on factor VIII and fibrinogen in man. Journal of Clinical Investigation. 48(4). 768–774. 5 indexed citations

Rankless uses publication and citation data sourced from OpenAlex, an open and comprehensive bibliographic database. While OpenAlex provides broad and valuable coverage of the global research landscape, it—like all bibliographic datasets—has inherent limitations. These include incomplete records, variations in author disambiguation, differences in journal indexing, and delays in data updates. As a result, some metrics and network relationships displayed in Rankless may not fully capture the entirety of a scholar's output or impact.

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