Amel Hamdi
Impact in
- Hematology top 10%
- Iron Metabolism and Disorders
-
- Hemoglobinopathies and Related Disorders
Papers in
- Genetics 7
- Hemoglobinopathies and Related Disorders 7
-
- Ubiquitin and proteasome pathways 2
- Heme Oxygenase-1 and Carbon Monoxide 2
- Co-authors
- Pierre Colas (4 shared papers)Prem Ponka (7 shared papers)Alex D. Sheftel (4 shared papers)Tariq Roshan (4 shared papers)Anne B. Mason (1 shared paper)Tanya Kahawita (1 shared paper)Daniel Garcia‐Santos (4 shared papers)Monika Horváthová (2 shared papers)
- Journals
- Blood (6 papers)Biotechnology Journal (1 paper)Indian Journal of Pharmaceutical Sciences (1 paper)Antiviral Research (1 paper)Frontiers in Immunology (1 paper)
- Partner nations
- CanadaFranceUnited Arab Emirates
In The Last Decade
Amel Hamdi
11 papers receiving 252 citations
Peers
Comparison fields: 5 of 56
- Hematology 61
- Genetics 49
- Cell Biology 40
- Nutrition and Dietetics 34
- Virology 10
Countries citing papers authored by Amel Hamdi
This map shows the geographic impact of Amel Hamdi'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 Amel Hamdi with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Amel Hamdi more than expected).
Fields of papers citing papers by Amel Hamdi
This network shows the impact of papers produced by Amel Hamdi. 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 Amel Hamdi. The network helps show where Amel Hamdi may publish in the future.
Co-authors
The 25 scholars most cited alongside Amel Hamdi, linked wherever they have co-authored with each other. Click a name or a connecting line to browse the papers they share.
All Works
| # | Work | ||
|---|---|---|---|
| 1 | 2016 | 100 | |
| 2 | 2011 | 72 | |
| 3 | 2017 | 34 | |
| 4 | 2011 | 25 | |
| 5 | 2012 | 10 | |
| 6 | 2015 | 4 | |
| 7 | 2022 | 3 | |
| 8 | 2015 | 3 | |
| 9 | 2015 | 2 | |
| 10 | 2014 | 2 | |
| 11 | 2015 | 1 | |
| 12 | 2016 | 1 | |
| 13 | 2025 | 0 | |
| 14 | 2024 | 0 | |
| 15 | 2025 | 0 |
About Amel Hamdi
Amel Hamdi is a scholar working on Genetics, Molecular Biology, Hematology, Physiology and Pharmacology, having authored 15 papers that have together received 257 indexed citations. Recurring topics across this work include Hemoglobinopathies and Related Disorders (7 papers), Iron Metabolism and Disorders (5 papers), Erythrocyte Function and Pathophysiology (5 papers), Ubiquitin and proteasome pathways (2 papers), Microtubule and mitosis dynamics (2 papers), Cancer-related Molecular Pathways (2 papers), Neonatal Health and Biochemistry (2 papers) and Heme Oxygenase-1 and Carbon Monoxide (2 papers). The work is most often cited by research in Hematology (61 citations), Genetics (49 citations), Cell Biology (40 citations), Nutrition and Dietetics (34 citations) and Virology (10 citations). Amel Hamdi has collaborated with scholars based in Canada, France and United Arab Emirates. Frequent co-authors include Pierre Colas, Prem Ponka, Alex D. Sheftel, Tariq Roshan, Anne B. Mason, Tanya Kahawita, Daniel Garcia‐Santos, Monika Horváthová, Carine Fillebeen and Kostas Pantopoulos. Their work appears in journals such as Blood, Biotechnology Journal, Indian Journal of Pharmaceutical Sciences, Antiviral Research and Frontiers in Immunology.
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.