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M

M.E. Truckenmiller

Researcher at Pennsylvania State University

Publications -  26
Citations -  957

M.E. Truckenmiller is an academic researcher from Pennsylvania State University. The author has contributed to research in topics: Antigen & Cytotoxic T cell. The author has an hindex of 19, co-authored 26 publications receiving 925 citations. Previous affiliations of M.E. Truckenmiller include National Institutes of Health & University of Washington.

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N-Acetylation of L-aspartate in the nervous system: differential distribution of a specific enzyme

TL;DR: L‐Aspartate N‐ acetyltransferase, a nervous system enzyme that mediates the synthesis of N‐acetyl‐L‐aspartic acid, has been characterized and found to be membrane‐associated and was solubilized by treatment with Triton X‐100.
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Crosstalk between the type 1 interferon and nuclear factor kappa B pathways confers resistance to a lethal virus infection.

TL;DR: It is shown that NF-κB is essential for resistance to ectromelia virus (ECTV), a mouse orthopoxvirus related to the virus causing human smallpox, and overlap between the T1-IFN and NF-σB pathways allows the host to overcome genetic or pathogen-induced deficiencies in T 1-IFn and survive an otherwise lethal poxvirus infection.
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Corticosterone impairs dendritic cell maturation and function.

TL;DR: It is found that physiologically relevant concentrations of CORT, acting via the glucocorticoid receptor, functionally compromise DC maturation, offering a potential mechanism underlying stress‐associated immunosuppression.
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Infection of rabbits with human immunodeficiency virus 1. A small animal model for acquired immunodeficiency syndrome

TL;DR: Examination of organs taken at necropsy from both HIV-1- and HTLV-1/HIV- 1-infected animals showed splenic hyperplasia and lymphocyte infiltration of the lungs, as well as moderate damage to liver and kidney in some cases.
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The dual role of CD8+ T lymphocytes in the development of stress-induced herpes simplex encephalitis.

TL;DR: It is suggested that a delayed infiltration of CD8(+) T cells into the brain may promote HSE in naive mice, while the presence of HSV-specific T cells in the brain prior to HSV challenge is protective, possibly by limiting HSV replication and spread within the CNS.