Donald C. Anderson
- Immunology top 1%
- Immunology and Allergy top 0.2%
- Molecular Biology top 10%
- Surgery top 5%
- Epidemiology top 5%
- Co-authors
- D. Neil GrangerRalph D. FeiginJulián PanésMasayuki MiyasakaFrank C. SchmalstiegMichael J. EppihimerTimothy A. SpringerMichael Chopp
- Topics
- Cell Adhesion Molecules Research (30 papers)Neutrophil, Myeloperoxidase and Oxidative Mechanisms (11 papers)Blood disorders and treatments (8 papers)
- Partner nations
- United StatesSpainJapan
In The Last Decade
Donald C. Anderson
89 papers receiving 4.8k citations
Peers
Comparison fields: 5 of 142
- Immunology 1.7k
- Immunology and Allergy 1.2k
- Molecular Biology 1.1k
- Surgery 773
- Epidemiology 668
Countries citing papers authored by Donald C. Anderson
This map shows the geographic impact of Donald C. Anderson'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 Donald C. Anderson with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Donald C. Anderson more than expected).
Fields of papers citing papers by Donald C. Anderson
This network shows the impact of papers produced by Donald C. Anderson. 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 Donald C. Anderson. The network helps show where Donald C. Anderson may publish in the future.
Co-authorship network of co-authors of Donald C. Anderson
This figure shows the co-authorship network connecting the top 25 collaborators of Donald C. Anderson. A scholar is included among the top collaborators of Donald C. Anderson 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 Donald C. Anderson. Donald C. Anderson is excluded from the visualization to improve readability, since they are connected to all nodes in the network.
All Works
| # | Work | Indexed citations |
|---|---|---|
| 1 | 156 | |
| 2 | 31 | |
| 3 | 78 | |
| 4 | 60 | |
| 5 | 60 | |
| 6 | 122 | |
| 7 | 38 | |
| 8 | 107 | |
| 9 | 43 | |
| 10 | 64 | |
| 11 | 217 | |
| 12 | Animal model of human disease: Bovine leukocyte adhesion deficiency: Beta2 Integrin Deficiency in Young Holstein Cattle | 10 |
| 13 | 81 | |
| 14 | 21 | |
| 15 | 23 | |
| 16 | 2 | |
| 17 | 57 | |
| 18 | 114 | |
| 19 | 4 | |
| 20 | 72 |
About Donald C. Anderson
Donald C. Anderson is a scholar working on Immunology and Allergy, Immunology and Hematology, having authored 94 papers that have together received 5.1k indexed citations. Recurring topics across this work include Cell Adhesion Molecules Research (30 papers), Neutrophil, Myeloperoxidase and Oxidative Mechanisms (11 papers) and Blood disorders and treatments (8 papers). The work is most often cited by research in Immunology and Allergy (1.2k citations), Immunology (1.7k citations) and Neurology (407 citations). Donald C. Anderson has collaborated with scholars based in United States, Spain and Japan. Frequent co-authors include D. Neil Granger, Ralph D. Feigin, Julián Panés, Masayuki Miyasaka, Frank C. Schmalstieg, Michael J. Eppihimer, Timothy A. Springer, Michael Chopp, Takashi Kishimoto and Barry A. Wolitzky. Their work appears in journals such as Science, Cell and JAMA.
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.