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Journal Article

Citation

Hayashi T, Nakamae T, Higo E, Ikematsu K, Ogata M. Leg. Med. (Elsevier) 2017; 24: 24-31.

Affiliation

Department of Legal Medicine, Graduate School of Medical and Dental Sciences, Kagoshima University, 8-35-1 Sakuragaoka, Kagoshima 890-8544, Japan. Electronic address: ogatam@m.kufm.kagoshima-u.ac.jp.

Copyright

(Copyright © 2017, Japanese Society of Legal Medicine, Publisher Elsevier Publishing)

DOI

10.1016/j.legalmed.2016.11.003

PMID

28081787

Abstract

Physical abuse of the elderly induces a massive primed neutrophil infiltration into the lung and liver through chemotaxis by interleukin (IL)-8, similar to cases of traumatic or hemorrhagic shock. Here, we used immunohistochemical analyses to investigate this infiltration in cases of physically abused children. In addition, we examined the expression of neutrophil elastase (NE) as the inflammatory mediator and α1-antitrypsin (AAT) as the elastase inhibitor. The number of neutrophils in the abuse cases was increased significantly in the heart, lung, liver, and kidney, compared with that of control cases. IL-8-positive cells and NE-positive cells in all organs of abuse cases were significantly greater than those in control cases. Large quantities of oxidized AAT, which fails to inactivate NE and results in tissue damage, was detected in the liver of abuse cases. Neutrophil infiltration showed positive correlation with the degree of systemic accumulation of non-fatal injuries caused by repetitive abusive behavior. Although further investigation using more autopsy samples is necessary, results of our preliminary study indicate that massive neutrophil infiltration induced by IL-8 in multiple organs is a new complementary diagnostic indicator of physical abuse in children. Moreover, the demonstration of NE-positive cells and oxidized AAT provides firm evidence of tissue damage.

Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.


Language: en

Keywords

Child physical abuse; Interleukin (IL)-8; Neutrophil elastase (NE); Oxidized α1-antitrypsin (AAT); Primed neutrophil infiltration

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