Tesfahun Desta

2.3k total citations
20 papers, 1.9k citations indexed

About

Tesfahun Desta is a scholar working on Periodontics, Molecular Biology and Rehabilitation. According to data from OpenAlex, Tesfahun Desta has authored 20 papers receiving a total of 1.9k indexed citations (citations by other indexed papers that have themselves been cited), including 15 papers in Periodontics, 6 papers in Molecular Biology and 5 papers in Rehabilitation. Recurrent topics in Tesfahun Desta's work include Oral microbiology and periodontitis research (15 papers), Immune Response and Inflammation (5 papers) and Wound Healing and Treatments (5 papers). Tesfahun Desta is often cited by papers focused on Oral microbiology and periodontitis research (15 papers), Immune Response and Inflammation (5 papers) and Wound Healing and Treatments (5 papers). Tesfahun Desta collaborates with scholars based in United States, Myanmar and China. Tesfahun Desta's co-authors include Dana T. Graves, Yugal Behl, Rongkun Liu, Ghada H. Naguib, Hesham Almashat, Sayon Roy, Salomon Amar, Qingxian Luan, Hongbing He and Takahiro Chino and has published in prestigious journals such as The Journal of Immunology, Diabetes and Endocrinology.

In The Last Decade

Tesfahun Desta

20 papers receiving 1.9k citations

Peers

Tesfahun Desta
Mani Alikhani United States
N.S. Ramamurthy United States
T. F. McNamara United States
Antonio Zizzi Italy
Juan Du China
L M Golub United States
Aarne Oikarinen Finland
Nicole Pischon Germany
Kyoung‐Jin Chung Germany
Mikihito Kajiya Japan
Mani Alikhani United States
Tesfahun Desta
Citations per year, relative to Tesfahun Desta Tesfahun Desta (= 1×) peers Mani Alikhani

Countries citing papers authored by Tesfahun Desta

Since Specialization
Citations

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

Fields of papers citing papers by Tesfahun Desta

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Tesfahun Desta. 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 Tesfahun Desta. The network helps show where Tesfahun Desta may publish in the future.

Co-authorship network of co-authors of Tesfahun Desta

This figure shows the co-authorship network connecting the top 25 collaborators of Tesfahun Desta. A scholar is included among the top collaborators of Tesfahun Desta 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 Tesfahun Desta. Tesfahun Desta 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.
Desta, Tesfahun, Jing Li, Takahiro Chino, & Dana T. Graves. (2010). Altered Fibroblast Proliferation and Apoptosis in Diabetic Gingival Wounds. Journal of Dental Research. 89(6). 609–614. 92 indexed citations
2.
Siqueira, Michelle F., Jialin Li, Leena Chehab, et al.. (2009). Impaired wound healing in mouse models of diabetes is mediated by TNF-α dysregulation and associated with enhanced activation of forkhead box O1 (FOXO1). Diabetologia. 53(2). 378–388. 175 indexed citations
3.
4.
Liu, Rongkun, et al.. (2008). P. gingivalis and E. coli Lipopolysaccharides Exhibit Different Systemic but Similar Local Induction of Inflammatory Markers. Journal of Periodontology. 79(7). 1241–1247. 61 indexed citations
5.
6.
Luan, Qingxian, Tesfahun Desta, Leena Chehab, et al.. (2008). Inhibition of Experimental Periodontitis by a Topical Boron-based Antimicrobial. Journal of Dental Research. 87(2). 148–152. 73 indexed citations
7.
Behl, Yugal, Michelle F. Siqueira, Jingchao Li, et al.. (2008). Activation of the Acquired Immune Response Reduces Coupled Bone Formation in Response to a Periodontal Pathogen. The Journal of Immunology. 181(12). 8711–8718. 57 indexed citations
8.
Desta, Tesfahun & Dana T. Graves. (2007). Fibroblast apoptosis induced by Porphyromonas gingivalis is stimulated by a gingipain and caspase-independent pathway that involves apoptosis-inducing factor. Cellular Microbiology. 9(11). 2667–2675. 33 indexed citations
9.
Liu, Rongkun, et al.. (2006). Tumor Necrosis Factor-α Mediates Diabetes-Enhanced Apoptosis of Matrix-Producing Cells and Impairs Diabetic Healing. American Journal Of Pathology. 168(3). 757–764. 100 indexed citations
10.
Zhou, Qingde, Tesfahun Desta, Matthew J. Fenton, Dana T. Graves, & Salomon Amar. (2006). Cytokine Profiling of Macrophages Exposed to Porphyromonas gingivalis , Its Lipopolysaccharide, or Its FimA Protein. Infection and Immunity. 74(3). 1995–1995. 2 indexed citations
11.
Leone, Cataldo, David Kuo, Tesfahun Desta, et al.. (2006). Immunization Enhances Inflammation and Tissue Destruction in Response toPorphyromonas gingivalis. Infection and Immunity. 74(4). 2286–2292. 27 indexed citations
12.
Bal, H. S., et al.. (2006). Diabetes Enhances Periodontal Bone Loss through Enhanced Resorption and Diminished Bone Formation. Journal of Dental Research. 85(6). 510–514. 225 indexed citations
13.
Almashat, Hesham, et al.. (2006). Diabetes Enhances mRNA Levels of Proapoptotic Genes and Caspase Activity, Which Contribute to Impaired Healing. Diabetes. 55(2). 487–495. 72 indexed citations
14.
Graves, Dana T., Ghada H. Naguib, Huafei Lü, Tesfahun Desta, & Salomon Amar. (2005). <I>Porphyromonas gingivalis</I> fimbriae are pro-inflammatory but do not play a prominent role in the innate immune response to <I>P. gingivalis</I>. Journal of Endotoxin Research. 11(1). 13–18. 16 indexed citations
15.
Zhou, Qingde, Tesfahun Desta, Matthew J. Fenton, Dana T. Graves, & Salomon Amar. (2005). Cytokine Profiling of Macrophages Exposed toPorphyromonas gingivalis, Its Lipopolysaccharide, or Its FimA Protein. Infection and Immunity. 73(2). 935–943. 180 indexed citations
16.
Graves, Dana T., Ghada H. Naguib, Huafei Lü, Tesfahun Desta, & Salomon Amar. (2005). Porphyromonas gingivalis fimbriae are pro-inflammatory but do not play a prominent role in the innate immune response to P. gingivalis. Journal of Endotoxin Research. 11(1). 13–18. 11 indexed citations
17.
Naguib, Ghada H., Hesham Almashat, Tesfahun Desta, & Dana T. Graves. (2004). Diabetes Prolongs the Inflammatory Response to a Bacterial Stimulus Through Cytokine Dysregulation. Journal of Investigative Dermatology. 123(1). 87–92. 187 indexed citations
18.
Liu, Rongkun, Tesfahun Desta, Hongbing He, & Dana T. Graves. (2004). Diabetes Alters the Response to Bacteria by Enhancing Fibroblast Apoptosis. Endocrinology. 145(6). 2997–3003. 56 indexed citations
19.
He, Hongbing, Rongkun Liu, Tesfahun Desta, et al.. (2003). Diabetes Causes Decreased Osteoclastogenesis, Reduced Bone Formation, and Enhanced Apoptosis of Osteoblastic Cells in Bacteria Stimulated Bone Loss. Endocrinology. 145(1). 447–452. 153 indexed citations
20.
Graves, Dana T., et al.. (2001). Tumor Necrosis Factor Modulates Fibroblast Apoptosis, PMN Recruitment, and Osteoclast Formation in Response to P. gingivalis Infection. Journal of Dental Research. 80(10). 1875–1879. 116 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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