D-Index & Metrics Best Publications

D-Index & Metrics D-index (Discipline H-index) only includes papers and citation values for an examined discipline in contrast to General H-index which accounts for publications across all disciplines.

Discipline name D-index D-index (Discipline H-index) only includes papers and citation values for an examined discipline in contrast to General H-index which accounts for publications across all disciplines. Citations Publications World Ranking National Ranking
Biology and Biochemistry D-index 66 Citations 21,456 297 World Ranking 3738 National Ranking 242

Overview

What is he best known for?

The fields of study he is best known for:

  • Internal medicine
  • Gene
  • Mutation

Ikuya Nonaka spends much of his time researching Muscular dystrophy, Internal medicine, Endocrinology, Genetics and Molecular biology. His Muscular dystrophy research incorporates themes from Duchenne muscular dystrophy and Skeletal muscle. His Internal medicine study integrates concerns from other disciplines, such as Collagen VI, Bethlem myopathy, Ullrich congenital muscular dystrophy and Respiratory chain.

Basal lamina is closely connected to Laminin in his research, which is encompassed under the umbrella topic of Molecular biology. The various areas that Ikuya Nonaka examines in his Dystrophin study include Immunofluorescence and Pathology. His study in Mitochondrial myopathy is interdisciplinary in nature, drawing from both Encephalopathy and Heteroplasmy.

His most cited work include:

  • A mutation in the tRNA Leu(UUR) gene associated with the MELAS subgroup of mitochondrial encephalomyopathies (1611 citations)
  • Mitochondrial DNA Deletions in Progressive External Ophthalmoplegia and Kearns-Sayre Syndrome (828 citations)
  • Myogenin gene disruption results in perinatal lethality because of severe muscle defect (771 citations)

What are the main themes of his work throughout his whole career to date?

His primary areas of investigation include Pathology, Internal medicine, Endocrinology, Myopathy and Muscular dystrophy. His research brings together the fields of Anatomy and Pathology. Ikuya Nonaka works mostly in the field of Internal medicine, limiting it down to topics relating to Mitochondrial myopathy and, in certain cases, Cytochrome c oxidase.

As a part of the same scientific family, Ikuya Nonaka mostly works in the field of Myopathy, focusing on Mutation and, on occasion, Mitochondrial DNA. His work deals with themes such as Limb-girdle muscular dystrophy and Laminin, which intersect with Muscular dystrophy. His research investigates the connection between Skeletal muscle and topics such as Molecular biology that intersect with problems in Biochemistry.

He most often published in these fields:

  • Pathology (35.50%)
  • Internal medicine (25.08%)
  • Endocrinology (21.17%)

What were the highlights of his more recent work (between 2009-2021)?

  • Pathology (35.50%)
  • Myopathy (20.85%)
  • Internal medicine (25.08%)

In recent papers he was focusing on the following fields of study:

Ikuya Nonaka mainly investigates Pathology, Myopathy, Internal medicine, Muscular dystrophy and Endocrinology. In his study, which falls under the umbrella issue of Pathology, Limb-girdle muscular dystrophy, Vacuole and Electromyography is strongly linked to Anatomy. His Myopathy study is associated with Genetics.

The Internal medicine study combines topics in areas such as Surgery, Weakness and Cardiology. The study incorporates disciplines such as Rimmed vacuoles, Pediatrics and Muscle pathology in addition to Muscular dystrophy. His study in Skeletal muscle, Muscle atrophy and Myocyte are all subfields of Endocrinology.

Between 2009 and 2021, his most popular works were:

  • Dominant mutations in ORAI1 cause tubular aggregate myopathy with hypocalcemia via constitutive activation of store-operated Ca2+ channels (95 citations)
  • Biallelic Mutations in MYPN, Encoding Myopalladin, Are Associated with Childhood-Onset, Slowly Progressive Nemaline Myopathy. (48 citations)
  • Characterization of the Asian myopathy patients with VCP mutations. (48 citations)

In his most recent research, the most cited papers focused on:

  • Internal medicine
  • Gene
  • Mutation

His scientific interests lie mostly in Internal medicine, Myopathy, Pathology, Muscular dystrophy and Endocrinology. His Myopathy study combines topics in areas such as Cytoplasm, Cytoplasmic inclusion, Mutation, Phenotype and Cerebellar ataxia. His Mutation research is included under the broader classification of Genetics.

His Pathology research is multidisciplinary, relying on both Hypotonia, Anatomy and Muscle pathology. His studies examine the connections between Muscular dystrophy and genetics, as well as such issues in Pediatrics, with regards to PTRF. His Endocrinology research integrates issues from Muscle biopsy, Sialic acid and Multiple Acyl-CoA Dehydrogenase Deficiency.

This overview was generated by a machine learning system which analysed the scientist’s body of work. If you have any feedback, you can contact us here.

Best Publications

A mutation in the tRNA Leu(UUR) gene associated with the MELAS subgroup of mitochondrial encephalomyopathies

Yu-Ichi Goto;Ikuya Nonaka;Satoshi Horai.
Nature (1990)

2610 Citations

Myogenin gene disruption results in perinatal lethality because of severe muscle defect

Yoko Nabeshima;Kazunori Hanaoka;Michiko Hayasaka;Eisaku Esuml.
Nature (1993)

1216 Citations

Mitochondrial DNA Deletions in Progressive External Ophthalmoplegia and Kearns-Sayre Syndrome

Carlos T. Moraes;Salvatore Dimauro;Massimo Zeviani;Anne Lombes.
The New England Journal of Medicine (1989)

1126 Citations

An ancient retrotransposal insertion causes Fukuyama-type congenital muscular dystrophy

Kazuhiro Kobayashi;Yutaka Nakahori;Masashi Miyake;Kiichiro Matsumura.
Nature (1998)

1047 Citations

Primary LAMP-2 deficiency causes X-linked vacuolar cardiomyopathy and myopathy (Danon disease)

Ichizo Nishino;Jin Fu;Kurenai Tanji;Takeshi Yamada.
Nature (2000)

909 Citations

Introduction of disease-related mitochondrial DNA deletions into HeLa cells lacking mitochondrial DNA results in mitochondrial dysfunction.

Jun-Ichi Hayashi;Shigeo Ohta;Aiko Kikuchi;Masakazu Takemitsu.
Proceedings of the National Academy of Sciences of the United States of America (1991)

710 Citations

Immunostaining of skeletal and cardiac muscle surface membrane with antibody against Duchenne muscular dystrophy peptide.

K Arahata;S Ishiura;T Ishiguro;T Tsukahara.
Nature (1988)

682 Citations

Mutations in the dystrophin-associated protein γ-sarcoglycan in chromosome 13 muscular dystrophy

Satoru Noguchi;Elizabeth M. McNally;Kamel Ben Othmane;Yasuko Hagiwara.
Science (1995)

608 Citations

Inter-mitochondrial complementation: Mitochondria-specific system preventing mice from expression of disease phenotypes by mutant mtDNA

Kazuto Nakada;Kimiko Inoue;Kimiko Inoue;Tomoko Ono;Kotoyo Isobe.
Nature Medicine (2001)

539 Citations

Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke‐like episodes (MELAS) A correlative study of the clinical features and mitochondrial DNA mutation

Y. Goto;S. Horai;T. Matsuoka;Y. Koga.
Neurology (1992)

506 Citations

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