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
Microbiology D-index 60 Citations 13,277 130 World Ranking 2051 National Ranking 861

Overview

What is he best known for?

The fields of study he is best known for:

  • Enzyme
  • Gene
  • Immune system

Heinz G. Remold focuses on Macrophage, Apoptosis, Molecular biology, Mycobacterium tuberculosis and Microbiology. His Macrophage research incorporates elements of Calcitonin, Endocrinology, Phagocytosis and Plasma membrane repair, Cell membrane. The Apoptosis study combines topics in areas such as Necrosis, Tumor necrosis factor alpha and Cell biology.

His Molecular biology study combines topics from a wide range of disciplines, such as In vitro, Macrophage migration inhibitory factor, Chemotaxis, Immunology and Binding site. His biological study spans a wide range of topics, including Virology, Antigen presentation, Immunity and Virulence. He works mostly in the field of Microbiology, limiting it down to topics relating to Intracellular and, in certain cases, Cytolysis and Caspase 3.

His most cited work include:

  • Virulent Mycobacterium tuberculosis Strains Evade Apoptosis of Infected Alveolar Macrophages (453 citations)
  • Infection by Mycobacterium tuberculosis promotes human alveolar macrophage apoptosis. (439 citations)
  • Pathogenic Mycobacterium tuberculosis evades apoptosis of host macrophages by release of TNF-R2, resulting in inactivation of TNF-alpha (348 citations)

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

Heinz G. Remold mainly focuses on Molecular biology, Macrophage, Biochemistry, Immunology and Microbiology. His Molecular biology research incorporates themes from Macrophage migration inhibitory factor, Lymphokine, Antigen, Peripheral blood mononuclear cell and Sephadex. His Macrophage research includes elements of Apoptosis, Cell, Receptor and Cell biology.

Concanavalin A is closely connected to Guinea pig in his research, which is encompassed under the umbrella topic of Biochemistry. His Immunology research focuses on subjects like Chemotaxis, which are linked to Cell Migration Inhibition and In vitro. His work deals with themes such as Tumor necrosis factor alpha, Cytokine, Mycobacterium, Virology and Mycobacterium tuberculosis, which intersect with Microbiology.

He most often published in these fields:

  • Molecular biology (42.21%)
  • Macrophage (37.66%)
  • Biochemistry (27.92%)

What were the highlights of his more recent work (between 2005-2021)?

  • Cell biology (19.48%)
  • Apoptosis (14.94%)
  • Necrosis (7.14%)

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

The scientist’s investigation covers issues in Cell biology, Apoptosis, Necrosis, Macrophage and Microbiology. His work carried out in the field of Cell biology brings together such families of science as Inflammation, Secretion and T cell. His research ties Molecular biology and Apoptosis together.

His work carried out in the field of Macrophage brings together such families of science as Intracellular, Programmed cell death and Plasma membrane repair. His Microbiology research is multidisciplinary, relying on both Annexin A1, Virology, Virulence and Mycobacterium tuberculosis. His Mycobacterium tuberculosis research includes elements of Antigen presentation and Immunity.

Between 2005 and 2021, his most popular works were:

  • Evasion of innate immunity by Mycobacterium tuberculosis : is death an exit strategy? (285 citations)
  • Apoptosis is an innate defense function of macrophages against Mycobacterium tuberculosis (264 citations)
  • Mycobacterium tuberculosis evades macrophage defenses by inhibiting plasma membrane repair (255 citations)

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

  • Enzyme
  • Gene
  • Immune system

His primary scientific interests are in Necrosis, Apoptosis, Macrophage, Cell biology and Immunity. Heinz G. Remold works mostly in the field of Necrosis, limiting it down to concerns involving Prostaglandin E and, occasionally, Lipoxin, Lipid signaling and Prostaglandin E synthase. Much of his study explores Macrophage relationship to Plasma membrane repair.

His study in Cell biology is interdisciplinary in nature, drawing from both Tumor necrosis factor alpha, T cell, Inflammation and Programmed cell death. Heinz G. Remold has included themes like Acquired immune system, Innate immune system and Tuberculosis in his Immunity study. His work on Microbiology expands to the thematically related Mycobacterium tuberculosis.

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

Virulent Mycobacterium tuberculosis Strains Evade Apoptosis of Infected Alveolar Macrophages

Joseph Keane;Heinz G. Remold;Hardy Kornfeld.
Journal of Immunology (2000)

677 Citations

Infection by Mycobacterium tuberculosis promotes human alveolar macrophage apoptosis.

J Keane;M K Balcewicz-Sablinska;H G Remold;G L Chupp.
Infection and Immunity (1997)

663 Citations

Pathogenic Mycobacterium tuberculosis evades apoptosis of host macrophages by release of TNF-R2, resulting in inactivation of TNF-alpha

Balcewicz-Sablinska Mk;Keane J;Kornfeld H;Remold Hg.
Journal of Immunology (1998)

527 Citations

Molecular cloning of a cDNA encoding a human macrophage migration inhibitory factor.

Weishui Y. Weiser;Patricia A. Temple;Joann S. Witek-Giannotti;Heinz G. Remold.
Proceedings of the National Academy of Sciences of the United States of America (1989)

492 Citations

Activation of human macrophages. Comparison of other cytokines with interferon-gamma.

C F Nathan;T J Prendergast;M E Wiebe;E R Stanley.
Journal of Experimental Medicine (1984)

468 Citations

Evasion of innate immunity by Mycobacterium tuberculosis : is death an exit strategy?

Samuel M. Behar;Maziar Divangahi;Maziar Divangahi;Heinz G. Remold.
Nature Reviews Microbiology (2010)

449 Citations

Apoptosis is an innate defense function of macrophages against Mycobacterium tuberculosis

Behar Sm;Martin Cj;Booty Mg;Nishimura T.
Mucosal Immunology (2011)

426 Citations

Lipid mediators in innate immunity against tuberculosis: opposing roles of PGE2 and LXA4 in the induction of macrophage death

Minjian Chen;Maziar Divangahi;Huixian Gan;Daniel S.J. Shin.
Journal of Experimental Medicine (2008)

390 Citations

Mycobacterium tuberculosis evades macrophage defenses by inhibiting plasma membrane repair

Maziar Divangahi;Minjian Chen;Huixian Gan;Danielle Desjardins.
Nature Immunology (2009)

388 Citations

Macrophage Apoptosis in Response to High Intracellular Burden of Mycobacterium tuberculosis Is Mediated by a Novel Caspase-Independent Pathway

Jinhee Lee;Heinz G. Remold;Michael H. Ieong;Hardy Kornfeld.
Journal of Immunology (2006)

318 Citations

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