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Joanna M. Matheson

Researcher at National Institute for Occupational Safety and Health

Publications -  13
Citations -  869

Joanna M. Matheson is an academic researcher from National Institute for Occupational Safety and Health. The author has contributed to research in topics: Tumor necrosis factor alpha & Toluene diisocyanate. The author has an hindex of 11, co-authored 12 publications receiving 840 citations.

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Deficiency of TNF receptors suppresses microglial activation and alters the susceptibility of brain regions to MPTP-induced neurotoxicity: role of TNF-alpha.

TL;DR: It is demonstrated that deficiency of TNF receptors suppresses microglial activation and alters the susceptibility of brain regions to MPTP‐induced neurotoxicity, indicative of a region‐specific and dual role for TNF‐α in the brain: a promoter of neurodegeneration in striatum and a protector against neurodegenersation in hippocampus.
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Toxic Metals Stimulate Inflammatory Cytokines in Hepatocytes through Oxidative Stress Mechanisms

TL;DR: These studies indicate that, in addition to other inflammatory mediators and acute phase proteins, cytokines and chemokines are produced by hepatocytes, which may participate in hepatotoxic responses.
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Tumor Necrosis Factor α and Toxicology

TL;DR: The molecular cloning of a group of proteins, collectively referred to as cytokines, including interleukins, chemokines, growth factors, colony stimulating factors, and tumor necrosis factors, has allowed for the increased understanding of the mechanisms for many disease processes as well as provided strategies for the development of novel therapies.
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Exposure and immunological determinants in a murine model for toluene diisocyanate (TDI) asthma.

TL;DR: Mice models for TDI asthma consistent with that found in workers with occupational asthma are described and indicate that the pulmonary pathology associated with TDI can vary depending upon the exposure paradigm.
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Polymorphisms of the IL-1 gene complex in coal miners with silicosis.

TL;DR: This is the first report showing an association between the IL-1RA (+ 2018) polymorphism and silicosis, and suggests that this polymorphism may confer increased risk for the development of the disease.