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Dod ( 376 ) Mp4 UPD


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Dod ( 376 ) mp4


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There are four different mechanisms of bodily damage after blast exposure. Primary blast injury is caused by the direct effect of the high pressure wave upon the tissue. Secondary blast injuries occur when the blast wind propels shell fragments or debris into the tissue. Tertiary blast injury is when the blast wind knocks down or blows the individual into a solid object. Quaternary blast injuries include all other effects, such as post-traumatic stress disorder or burns [4]. Primary blast injury is most noticeable where density changes markedly, such as tissue-air junctions [5]. Therefore, damage to the ear is a primary blast injury. Other organs that are particularly sensitive to primary blast injury include the lung and abdomen [6], [7].


The blast wave profile impacting each mouse was measured for every experiment using a high-speed pressure transducer (Model 102B16, PCB piezotronics, Depew, NY) that was positioned just below the mouse, 11 cm from the end of the tube. We collected the pressure data dynamically using a signal conditioner (Model 482A21, PCB piezotronics) and digital oscilloscope (Model TDS2014B, Tektronix, Beaverton, OR). Our chamber could generate peak pressures of up to 186 kPa, corresponding to a sound intensity of 199 dB SPL (sound pressure level) at the position of the mouse.


Both measurements demonstrated that there was an initial overpressure peak followed by a negative pressure phase. These data revealed that the blast wave conformed to the theoretical ideal for a blast wave as given by a Friedlander function [14]. There was an immediate rise at the onset of the blast that corresponds with the blast wave (0 ms) and the blast wind could be seen as the slower rise to the peak blast pressure (2 ms). The pressure then dropped below the baseline as the blast wave and wind propagated past the sensor and then slowly recovered. There were two small perturbations in the pressure signal (arrows) that originated from reflections of the blast wave. The duration of the blast was the time from the onset of the blast to the zero-crossing point (blue arrows). For all remaining experiments, only the stagnation pressure measurements were performed. A power spectral density analysis of five blasts was performed and averaged (inset,Fig. 1A). This demonstrated that most of the blast energy was below 1 kHz, although there was energy out to 12.5 kHz (the maximum frequency we could analyze based on sampling rate) and an energy peak at 5 kHz.


The minimum reservoir pressure necessary to move the components inside the chamber and produce a blast was roughly 345 kPa (50 psi). The maximum reservoir pressure we arbitrarily decided to limit to 793 kPa (115 psi). We then plotted representative blast wave profiles versus time at different reservoir pressures (Fig. 1B, C). This demonstrated that higher reservoir pressures produced higher blast pressures. As well, while the onset profile of the blast wave demonstrated a step response at higher reservoir pressures, there was an onset rise-time associated with the lower reservoir pressures (compare the first 1 ms of the bottom and top tracings in Fig. 1B). This indicates that the shock front had not developed as well when using lower pressures compared to higher pressures. Nevertheless, higher peak blast pressures were associated with slightly longer blast times (Fig. 1D), consistent with the production of higher magnitude blast waves and blast winds.


The blast peak pressure is given in the lower right of each plot. (A,B) The lowest blast pressure cohort had a nearly complete recovery of ABR thresholds and a partial recovery of DPOAE thresholds within two weeks. However there were still statistically significant differences between the ABR and DPOAE thresholds before the blast compared to 14 days after blast (two-way ANOVA, p


In the first cohort (942 kPa), ABR and DPOAE thresholds were substantially elevated immediately following the blast exposure (Day 0). These elevations were over the entire frequency spectrum. Over the subsequent two weeks, there was a gradual partial recovery of the thresholds. While the ABR thresholds nearly recovered completely in the lower frequencies (30 kHz). In contrast, the DPOAE thresholds demonstrated much larger elevations over the entire frequency spectrum. The other two cohorts (1239 and 1815 kPa) had ABR threshold shifts that demonstrated larger initial threshold elevations and less recovery. However, DPOAE thresholds showed little-to-no recovery over the frequency spectrum.


The sections were 10 µm thick. (A) The complete cochlear cross-sections are shown with labels indicating the areas that are enlarged. (B,C,D) Enlargements of the apical turn (B), the upper basal turn (C), and the lower basal turn (D). There was no evidence for obvious gross disruption of the intracochlear soft tissues. However, there was apparent loss of OHCs in the basal region of the cochlea as assessed by loss of their dark-stained nuclei (compare arrows in D). Scale bars: A-250 µm, B-50 µm.


OHCs are red and IHCs are green. (A) An age-matched control mouse demonstrates the full complement of OHCs and IHCs. Scale bar 100 µm. (B) Three months after blast-exposure, substantial OHC loss was found within the basal turn. While some IHCs were missing, most were present. The transition zone roughly 30% up from the base of the cochlea (arrow) marked the point at which some OHCs were able to survive the blast trauma. (C) Cytocochleograms were performed for quantification in mice three months after blast. (D) There were no differences in the patterns of OHC loss between the three rows in mice after blast. 041b061a72


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