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Hunter Phillips
Hunter Phillips

Dod ( 386 ) Mp4

The Defense Contract Management Agency provides contract administration services for the Department of Defense, other federal organizations and international partners, and is an essential part of the acquisition process from pre-award to sustainment.

Dod ( 386 ) mp4

Every business day, DCMA receives nearly 1,000 new contracts and authorizes more than $650 million in payments to contractors. Most importantly, every day the DCMA team delivers more than a million and a half items - from fighter jets to fasteners - to our warfighters.

MISSION We are the independent eyes and ears of DoD and its partners, enhancing warfighter lethality by ensuring timely delivery of quality products, and providing relevant acquisition insight supporting affordability and readiness.

While the tune THE FIRST NOEL is also a folk song, it did not appear in print until William Sandys's Christmas Carols, Ancient and Modern in 1833, with this text. According to Alan Luff, the melody may come from Cornwall, England, because Sandys transcribed it there, and because two other songs from that region are quite similar (The Hymnal 1982 Companion, vol. 3A, p. 223). The standard harmonization is from Stainer and Bramley's Christmas Carols New and Old, published in 1871.

RB rear rotor hats are made with iron sleeve liner and is fully compatible with OE rear drum brakes w/o having to delete it like other aftermarekt two piece rotors, or only machined from aluminum that can score and destroy the rotor hats if the parking brake is not released.

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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.

There was an orderly alignment of the three rows of OHCs and single row of IHCs. However, missing hair cells were easily identifiable as a lack of fluorescence. We counted the hair cells and created cytocochleograms to assess the relationship between hair cell loss and cochlear location (Fig. 5C,D). Hair cell loss was highest at the base and declined at more apical locations. In fact, there was no hair cell loss in the apical half of the cochlea. As well, the loss of OHCs was remarkably larger than the loss of IHCs. There was no difference in the degree of OHC loss between the three rows.

Residual OHCs seven days after blast exposure do not have gross disturbances of their stereociliary bundles. Asterisks indicate missing OHCs. (A,B) The apex of the cochlea. (C,D) The middle of the cochlea. (E, F) The base of the cochlea. While blast-exposed mice did not have any residual OHCs present within the far base of their cochlea, shown here is a cluster of residual OHCs at the transition zone (arrow in Fig. 5B). (G, H) Enlargements of the OHCs indicated by the white boxes in parts C&D. In all images, the normal stereociliary bundle morphology is seen. The scale bar is 8 µm.

To further characterize the injury, we labeled afferent synapses using antibodies to CtBP2, a structure associated with synaptic ribbons, which are found on the presynaptic (hair cell) side of the synapse. Antibodies to Tuj1 were also used to label the nerve fibers. While >95% of afferent synapses are associated with IHCs (to type I spiral ganglion neurons), there are some afferent synapses associated with OHCs as well (to type II spiral ganglion neurons) [21]. We focused our analysis on the apical and middle regions of the cochlea, as this is where there was no evidence of hair cell loss. We found a high density of punctate labeling along the IHCs and scattered punctate labeling along the OHCs in control mice (Fig. 7B). However, seven days after blast exposure (1815 kPa), there was an obvious decrease in the density of labeling under both IHCs and OHCs.

We performed Z-stacks, reconstructed them in 3D, and then carefully counted the number of fluorescent puncta associated with each IHC and OHC from two control and two blast exposed mice (two z-stacks were collected from each cochlea in both the 8 and 12 kHz regions). We found that there was a significant decrease in the number of synaptic ribbons associated with IHCs after blast exposure (7.690.43 vs. 12.460.42 per IHC). Similarly, there was a reduction in the number of synaptic ribbons associated with OHCs between the two cohorts (0.630.07 vs. 1.250.07 per OHC). This indicates that even though there was no hair cell loss in the apical region of the cochlea after blast exposure, there was loss of spiral ganglion innervation to that region. Because this large degree of loss was found in the apical regions of the cochlea and affected both IHCs and OHCs, the amount of loss we noted was more extensive than what has been shown in noise-exposed mice [22]. Nevertheless, the overall findings are consistent with what has been previously published, and indicates that the blast exposure not only leads to loss of afferent nerve fibers, but also produces changes in the intracellular molecular morphology of residual hair cells. 041b061a72


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