Investigations of Tissue-Level Mechanisms of Primary Blast Injury Through Modeling, Simulation, Neuroimaging and Neuropathological Studies

2012 ◽  
Author(s):  
R. Radovitzky ◽  
S. Socrate ◽  
K. Taber ◽  
R. Hurley ◽  
David Moore ◽  
...  
2019 ◽  
Vol 166 (E) ◽  
pp. e66-e69 ◽  
Author(s):  
Ying Liu ◽  
Y E Liu ◽  
C C Tong ◽  
P F Cong ◽  
X Y Shi ◽  
...  

IntroductionPrimary blast affects the kidneys due to direct shock wave damage and the production of proinflammatory cytokines without effective treatment. CD28 has been reported to be involved in regulating T cell activation and secretion of inflammatory cytokines. The aim of this study was to investigate the influence of primary blast on the kidney and the effect of CD28 in mice.MethodsA mouse model of primary blast-induced kidney injury was established using a custom-made explosive device. The severity of kidney injury was investigated by H&E staining. ELISA was applied to study serum inflammation factors’ expression. Western blot assays were used to analyse the primary blast-induced inflammatory factors’ expression in the kidney. Immunofluorescence analysis was used to examine the PI3K/Akt signalling pathway.ResultsHistological examination demonstrated that compared with the primary blast group, CD28 deficiency caused a significant decrease in the severity of the primary blast-induced renal injury. Moreover, ELISA and western blotting revealed that CD28 deficiency significantly reduced the levels of interleukin (IL)-1β, IL-4 and IL-6, and increased the IL-10 level (p<0.05). Finally, immunofluorescence analysis indicated that PI3K/Akt expression also changed.ConclusionsCD28 deficiency had protective effects on primary blast-induced kidney injury via the PI3K/Akt signalling pathway. These findings improve the knowledge on primary blast injury and provide theoretical basis for primary blast injury treatment.


2007 ◽  
Vol 25 (1) ◽  
pp. 97-98 ◽  
Author(s):  
Serkan Yılmaz ◽  
Murat Pekdemir
Keyword(s):  

2001 ◽  
Vol 166 (10) ◽  
pp. 918-920 ◽  
Author(s):  
Fred R. Sylvia ◽  
Angela I. Drake ◽  
Derin C. Wester
Keyword(s):  

2010 ◽  
Vol 251 (6) ◽  
pp. 1140-1144 ◽  
Author(s):  
Amber E. Ritenour ◽  
Lorne H. Blackbourne ◽  
Joseph F. Kelly ◽  
Daniel F. McLaughlin ◽  
Lisa A. Pearse ◽  
...  

2013 ◽  
Vol 30 (19) ◽  
pp. 1652-1663 ◽  
Author(s):  
Christopher D. Hue ◽  
Siqi Cao ◽  
Syed F. Haider ◽  
Kiet V. Vo ◽  
Gwen B. Effgen ◽  
...  

2011 ◽  
Vol 366 (1562) ◽  
pp. 286-290 ◽  
Author(s):  
E. Kirkman ◽  
S. Watts

Lung injuries, predominantly arising from blast exposure, are a clinical problem in a significant minority of current military casualties. This special feature consists of a series of articles on lung injury. This first article examines the mechanism of the response to blast lung (primary blast injury to the lung). Subsequent articles examine the incidence of blast lung, clinical consequences and current concepts of treatment, computer ( in silico ) modelling of lung injury and finally chemical injuries to the lungs. Blast lung is caused by a shock wave generated by an explosion causing widespread damage in the lungs, leading to intrapulmonary haemorrhage. This, and the ensuing inflammatory response in the lung, leads to a compromise in pulmonary gas exchange and hypoxia that can worsen over several hours. There is also a characteristic cardio-respiratory effect mediated via an autonomic reflex causing apnoea (or rapid shallow breathing), bradycardia and hypotension (the latter possibly also due to the release of nitric oxide). An understanding of this response, and the way it modifies other reflexes, can help the development of new treatment strategies for this condition and for the way it influences the patient's response to concomitant injuries.


2017 ◽  
Vol 70 (1) ◽  
pp. 104-105 ◽  
Author(s):  
John M. Wightman
Keyword(s):  

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