scholarly journals Air Blast Meshing & Pressure Mapping

2021 ◽  
Author(s):  
Gerrit Vander Wiel
Keyword(s):  
Air Blast ◽  
Pressure Mapping

scholarly journals Air Blast Mesh Sensitivity and Pressure Mapping Study

2021 ◽  
Author(s):  
Gerrit Vander Wiel ◽  
Paula Rutherford ◽  
Phillip Wolfram
Keyword(s):  
Mapping Study ◽  
Air Blast ◽  
Pressure Mapping ◽  
Mesh Sensitivity

scholarly journals Effects of intravitreal injection of siRNA against caspase-2 on retinal and optic nerve degeneration in air blast induced ocular trauma

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Chloe N. Thomas ◽  
Alexandra Bernardo-Colón ◽  
Ella Courtie ◽  
Gareth Essex ◽  
Tonia S. Rex ◽  
...  
Keyword(s):  
Intravitreal Injection ◽  
Fluorescent Protein ◽  
Ocular Trauma ◽  
Ganglion Cells ◽  
Intravitreal Injections ◽  
Nerve Degeneration ◽  
Injection Timing ◽  
Air Blast ◽  
Neuroprotective Therapy ◽  
Caspase 2

AbstractOcular repeated air blast injuries occur from low overpressure blast wave exposure, which are often repeated and in quick succession. We have shown that caspase-2 caused the death of retinal ganglion cells (RGC) after blunt ocular trauma. Here, we investigated if caspase-2 also mediates RGC apoptosis in a mouse model of air blast induced indirect traumatic optic neuropathy (b-ITON). C57BL/6 mice were exposed to repeated blasts of overpressure air (3 × 2 × 15 psi) and intravitreal injections of siRNA against caspase-2 (siCASP2) or against a control enhanced green fluorescent protein (siEGFP) at either 5 h after the first 2 × 15 psi (“post-blast”) or 48 h before the first blast exposure (“pre-blast”) and repeated every 7 days. RGC counts were unaffected by the b-ITON or intravitreal injections, despite increased degenerating ON axons, even in siCASP2 “post-blast” injection groups. Degenerating ON axons remained at sham levels after b-ITON and intravitreal siCASP2 “pre-blast” injections, but with less degenerating axons in siCASP2 compared to siEGFP-treated eyes. Intravitreal injections “post-blast” caused greater vitreous inflammation, potentiated by siCASP2, with less in “pre-blast” injected eyes, which was abrogated by siCASP2. We conclude that intravitreal injection timing after ocular trauma induced variable retinal and ON pathology, undermining our candidate neuroprotective therapy, siCASP2.

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