L. Feng

1.8k total citations
19 papers, 795 citations indexed

About

L. Feng is a scholar working on Molecular Biology, Cardiology and Cardiovascular Medicine and Genetics. According to data from OpenAlex, L. Feng has authored 19 papers receiving a total of 795 indexed citations (citations by other indexed papers that have themselves been cited), including 17 papers in Molecular Biology, 9 papers in Cardiology and Cardiovascular Medicine and 5 papers in Genetics. Recurrent topics in L. Feng's work include Muscle Physiology and Disorders (15 papers), Cardiomyopathy and Myosin Studies (9 papers) and Neurogenetic and Muscular Disorders Research (5 papers). L. Feng is often cited by papers focused on Muscle Physiology and Disorders (15 papers), Cardiomyopathy and Myosin Studies (9 papers) and Neurogenetic and Muscular Disorders Research (5 papers). L. Feng collaborates with scholars based in United Kingdom, Australia and United States. L. Feng's co-authors include Caroline A. Sewry, S. Brown, Francesco Muntoni, Eugenio Mercuri, Heinz Jungbluth, S. Robb, Maria Kinali, C. Jimenez‐Mallebrera, Francesco Muntoni and Martin Brockington and has published in prestigious journals such as Neurology, Neuropathology and Applied Neurobiology and Neuromuscular Disorders.

In The Last Decade

L. Feng

18 papers receiving 782 citations

Peers — A (Enhanced Table)

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

Name h Career Trend Papers Cites
L. Feng United Kingdom 13 674 254 187 122 107 19 795
Andoni Urtizberea France 15 555 0.8× 129 0.5× 155 0.8× 161 1.3× 203 1.9× 27 796
Susana Quijano‐Roy France 18 1.0k 1.5× 379 1.5× 276 1.5× 151 1.2× 233 2.2× 32 1.2k
Rita C.M. Pavanello Brazil 18 899 1.3× 254 1.0× 210 1.1× 108 0.9× 303 2.8× 50 1.0k
Akanchha Kesari United States 14 735 1.1× 161 0.6× 149 0.8× 94 0.8× 74 0.7× 20 853
Madoka Mori‐Yoshimura Japan 18 522 0.8× 213 0.8× 168 0.9× 109 0.9× 156 1.5× 87 881
I. Courdier-Fruh Switzerland 11 686 1.0× 105 0.4× 131 0.7× 118 1.0× 115 1.1× 13 829
Simon Guiraud United Kingdom 15 689 1.0× 108 0.4× 75 0.4× 96 0.8× 97 0.9× 18 782
Tiziana Mongini Italy 14 399 0.6× 117 0.5× 48 0.3× 103 0.8× 141 1.3× 46 595
Fédérica Piccolo United States 10 897 1.3× 238 0.9× 126 0.7× 259 2.1× 409 3.8× 21 969
Raffaella Brugnoni Italy 13 433 0.6× 158 0.6× 89 0.5× 74 0.6× 166 1.6× 25 557

Countries citing papers authored by L. Feng

Since Specialization
Citations

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

Fields of papers citing papers by L. Feng

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of L. Feng

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

All Works

19 of 19 papers shown
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Sewry, Caroline A., L. Feng, D. Chambers, Emma Matthews, & Rahul Phadke. (2021). Importance of immunohistochemical evaluation of developmentally regulated myosin heavy chains in human muscle biopsies. Neuromuscular Disorders. 31(5). 371–384. 7 indexed citations
3.
Phadke, Rahul, Anna Sárközy, Emily C. Oates, et al.. (2019). P.236Myofibres with subsarcolemmal rims and/or central aggregates of mitochondria (SRCAM) are prevalent in congenital titinopathies. Neuromuscular Disorders. 29. S135–S135.
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Illingworth, Marjorie, Marion Main, Matthew Pitt, et al.. (2014). RYR1-related congenital myopathy with fatigable weakness, responding to pyridostigimine. Neuromuscular Disorders. 24(8). 707–712. 31 indexed citations
7.
Maggi, Lorenzo, Mariacristina Scoto, Sebahattin Çirak, et al.. (2013). Congenital myopathies – Clinical features and frequency of individual subtypes diagnosed over a 5-year period in the United Kingdom. Neuromuscular Disorders. 23(3). 195–205. 96 indexed citations
8.
Clement, Emma, L. Feng, R. Mein, et al.. (2012). Relative frequency of congenital muscular dystrophy subtypes: Analysis of the UK diagnostic service 2001–2008. Neuromuscular Disorders. 22(6). 522–527. 41 indexed citations
9.
Kim, Jihee, C. Jimenez‐Mallebrera, A. Reghan Foley, et al.. (2011). Flow cytometry analysis: A quantitative method for collagen VI deficiency screening. Neuromuscular Disorders. 22(2). 139–148. 16 indexed citations
10.
Çirak, Sebahattin, Virginia Arechavala‐Gomeza, Michela Guglieri, et al.. (2011). P03 Exon skipping and dystrophin restoration in Duchenne muscular dystrophy patients after systemic phosphorodiamidate morpholino oligomer treatment. Neuromuscular Disorders. 21. S7–S8. 1 indexed citations
11.
Scoto, Mariacristina, Sebahattin Çirak, R. Mein, et al.. (2011). SEPN1 -related myopathies. Neurology. 76(24). 2073–2078. 57 indexed citations
12.
Munot, Pinki, Daniel Lashley, Heinz Jungbluth, et al.. (2010). Congenital fibre type disproportion associated with mutations in the tropomyosin 3 (TPM3) gene mimicking congenital myasthenia. Neuromuscular Disorders. 20(12). 796–800. 41 indexed citations
13.
Arechavala‐Gomeza, Virginia, Maria Kinali, L. Feng, et al.. (2009). Immunohistological intensity measurements as a tool to assess sarcolemma‐associated protein expression. Neuropathology and Applied Neurobiology. 36(4). 265–274. 66 indexed citations
14.
Muntoni, Francesco, Martin Brockington, C. Godfrey, et al.. (2007). Muscular dystrophies due to defective glycosylation of dystroglycan.. PubMed. 26(3). 129–35. 37 indexed citations
15.
Jimenez‐Mallebrera, C., Maria Antonietta Maioli, Jihee Kim, et al.. (2006). A comparative analysis of collagen VI production in muscle, skin and fibroblasts from 14 Ullrich congenital muscular dystrophy patients with dominant and recessive COL6A mutations. Neuromuscular Disorders. 16(9-10). 571–582. 75 indexed citations
16.
Torelli, Silvia, S. Brown, C. Jimenez‐Mallebrera, et al.. (2004). Absence of neuronal nitric oxide synthase (nNOS) as a pathological marker for the diagnosis of Becker muscular dystrophy with rod domain deletions. Neuropathology and Applied Neurobiology. 30(5). 540–545. 44 indexed citations
17.
Jungbluth, Heinz, C. R. Müller, B. Halliger–Keller, et al.. (2002). Autosomal recessive inheritance of RYR1 mutations in a congenital myopathy with cores. Neurology. 59(2). 284–287. 114 indexed citations
18.
Mercuri, Eugenio, Yeliz Yuva, S. Brown, et al.. (2002). Collagen VI involvement in Ullrich syndrome. Neurology. 58(9). 1354–1359. 74 indexed citations
19.
Sewry, Caroline A., S. Brown, Eugenio Mercuri, et al.. (2001). Skeletal muscle pathology in autosomal dominant Emery‐Dreifuss muscular dystrophy with lamin A/C mutations. Neuropathology and Applied Neurobiology. 27(4). 281–290. 89 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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