Daniel N. Mohler
- Physiology
- Hematology top 10%
- Pediatrics, Perinatology and Child Health top 10%
- Genetics top 10%
- Molecular Biology
- Co-authors
- David A. HorwitzCharles E. HessMunsey S. WhebyVirginia MinnichMichael D. GarrickPhilip W. MajerusWilliam J. WilliamsMichael Doukas
- Topics
- Erythrocyte Function and Pathophysiology (9 papers)Hemoglobinopathies and Related Disorders (4 papers)Blood groups and transfusion (3 papers)
- Cited by
- HematologyFamily PracticeGenetics
- Partner nations
- United StatesUnited Kingdom
In The Last Decade
Daniel N. Mohler
17 papers receiving 387 citations
Peers
Comparison fields: 5 of 94
- Physiology 129
- Hematology 100
- Pediatrics, Perinatology and Child Health 98
- Genetics 80
- Molecular Biology 63
Countries citing papers authored by Daniel N. Mohler
This map shows the geographic impact of Daniel N. Mohler'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 Daniel N. Mohler with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Daniel N. Mohler more than expected).
Fields of papers citing papers by Daniel N. Mohler
This network shows the impact of papers produced by Daniel N. Mohler. 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 Daniel N. Mohler. The network helps show where Daniel N. Mohler may publish in the future.
Co-authorship network of co-authors of Daniel N. Mohler
This figure shows the co-authorship network connecting the top 25 collaborators of Daniel N. Mohler. A scholar is included among the top collaborators of Daniel N. Mohler 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 Daniel N. Mohler. Daniel N. Mohler is excluded from the visualization to improve readability, since they are connected to all nodes in the network.
All Works
| # | Work | Indexed citations |
|---|---|---|
| 1 | 28 | |
| 2 | 15 | |
| 3 | Patients with hereditary spherocytosis may have clinically significant iron overload when they are also heterozygous for hemochromatosis. | 1 |
| 4 | 17 | |
| 5 | 95 | |
| 6 | 6 | |
| 7 | 72 | |
| 8 | 1 | |
| 9 | 3 | |
| 10 | 35 | |
| 11 | 25 | |
| 12 | 5 | |
| 13 | 25 | |
| 14 | 11 | |
| 15 | 10 | |
| 16 | 56 | |
| 17 | 95 |
About Daniel N. Mohler
Daniel N. Mohler is a scholar working on Genetics, Hematology and Physiology, having authored 17 papers that have together received 500 indexed citations. Recurring topics across this work include Erythrocyte Function and Pathophysiology (9 papers), Hemoglobinopathies and Related Disorders (4 papers) and Blood groups and transfusion (3 papers). The work is most often cited by research in Hematology (100 citations), Family Practice (18 citations) and Genetics (80 citations). Daniel N. Mohler has collaborated with scholars based in United States and United Kingdom. Frequent co-authors include David A. Horwitz, Charles E. Hess, Munsey S. Wheby, Virginia Minnich, Michael D. Garrick, Philip W. Majerus, William J. Williams, Michael Doukas, Carlos R. Ayers and William R. Sandusky. Their work appears in journals such as New England Journal of Medicine, Journal of Clinical Investigation and Blood.
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.