Couple of things was thinking on. Had a review of Prouty's
Secrete Teams - below it is a condensed interview version of what many are familiar with. It was a good reminder when he discusses the mechanism phases of assassination. The patsy, who one needs to forget as that is the obvious distraction (with planted so-called evidence salted around as part of the cover story, and than the teams. Generally, one team is the triangulation of guns - of gunmen, but the big story is in the aftermath coordination; who did what, said what, or appeared to do nothing obvious. This is the Achilles heel that gets noticed, and in Charlie's case, there were/are things to notice.
(Joe) So the device that was the manipulated mic on Charlie's shirt, it contained a small amount of explosives like C4?
A: Yes
The setup appears to be a shot (distraction) from Charlie's center to left side, that corresponds with the exit wound trauma on his neck, slightly left. As has been revealed here by the C's, the entry wound (not seen) traveled across from the right, below the shirt line, from the mic.
The distractions were immediatly put in play and the clean-up phase started.
Q: (Niall) And it was placed on him by a member of his security detail.
A: Yes
Had initially thought that Candace had said something about the person who affixed the mic on Charlie; a friend or someone she knows, was that it can be seen to correspond with the left side trauma, and to get that, the mic had to be angled/aimed? If affixing a mic, why not align it vertically? Would that be natural? Is the mic directed to be aimed that way as part of the mic pickup instruction? On Charlie, it was affixed at angle to the upper left. This could be a coincidence, or the manufactures directions, or it would not have mattered if the outcome had not been exactly what was seen. I don't know. However, being that the mic was affixed by a security detail person, Prouty had me thinking about it from what he had said, being part of a team.
Q: (Joe) And the people who made this, did they test it on someone beforehand?
A: Dummies.
The main question for me is: what is the minimum amount of energy necessary to produce the effects seen in Charlie's body? It's not just a matter of penetrating the body like a 9mm bullet (which Grok estimates to be about 200 joules - easily produced by a 1-2 cm shaped charge), but also the impact effects seen. In the opinion of a guy like Gary Melton at Paramount Tactical, he thinks that it looks like Charlie got hit by something as powerful as a .30-06 based on the way his chest caves, his face/neck deforms, etc. That's why he thinks he was wearing body armor - because the neck wound without an exit wound is not consistent with that amount of force.
So two related questions would be: Can that amount of energy be produced by a charge small enough to fit in the mic casing? And what is the maximum amount of energy that can be produced by a shaped charge of that size? Those questions might not be answerable for us if such a device used advanced technology for which there is no real precedent. But we might at least be able to get an idea if it is possible based on what is currently known about shaped charges.
My first thought regarding your main question - tied to the second and third question, might be that perhaps it depends on the arrangement of some of the variables. The assembly of whatever it was, needed to be mathematically down scaled and miniaturized to fit in a mic, and to mimic the ability to penetrate in terms of physics (assume this was done from a portion of the battery), and it would need focused direction. Perhaps the design template was mapped out mathematically using matching physics, 3d printed and copied using the right liner material and diameter, and enough c4 grains to fire either a jet of force, or a physical projectile, like a very small metal cap or EFP. It might really be smaller than a ladyfinger for those of you who fired them off as a kid, but without powder fuse, it needed an electronic initiator and direction.
Q: (Joe) And the automatic remote firing system for the rifle that fired the gunshot was in that general area where that kind of roof was, I suppose?
A: Yes
See EFP here and
Does Size Matter? | Explosive Shaped Charge Comparison (this guy is pretty good):
Here is a
paper Effect of tungsten contents on the jet penetration performance of shaped charge liner based copper Tungsten composites that may provide the math and physics. In one figure, H11 explosive was used, although its aim is on W-Cu composite liners.
Approaching Infinity, I don't know how small it can be brought down and still do what it did. Just could not find anything.
A: The explosion created a limited shock wave that was shaped and contained by the t-shirt itself allowing the shock to travel around his shoulders and torso.
Came across another
paper on
Understanding blast-induced neurotrauma: how far have we come?
This was weird to read, that they experimented with all this on all sorts of animals, yet points come up focused on blast waves and physical trauma of what happens in parts of the body. Note, this is not immediate death as was the case with Charlie, it is blast trauma.
There seems, no doubt, that there was a blast wave of some type as the forced jet/object entered Charlie from lower right to exit higher left. Here is what it says, and keep in mind this is exposure to a pressure wave, and in Charlie's case, it was small ("contained in the t-shirt"), yet directly against the body and than in the body if what happened had happened. This may help to explain the mass initial release of blood upon exit with propagation, and what the body was immediatly doing (severing the carotid artery is obviously part of it). This would also be by degree, yet by what happened, there was a shock wave inside Charlie's body:
Pathobiology
After the shock wave interacts with the body and head,
a pressure wave passes through the body and head inducing complex response mechanisms, which can be divided into four main groups:
primary tissue damage of the brain parenchyma caused by stretch, strain and/or rupture of parenchyma and blood vessels; changes triggered by the ANS; consequences of increased vascular load; and effects of locally synthesized and released mediators modulators (so-called ‘autacoids’) and/or immune system activation.
Primary tissue damage
The
propagation of the pressure wave, induced by the shock wave–body/head interaction,
causes a relative motion of tissue components that may tear the interfaces between parenchyma, blood vessels, fluid/blood and air. In lungs, alveolar rupture, thinning of alveolar septae, circumscribed subpleural, intra-alveolar and perivascular hemorrhages have been seen to develop as direct consequences of the shock wave induced primary tissue damage [
76,
77].
In the brain, the rupture of the bridging veins leads to the development of subarachnoid hemorrhage (SAH) [
78] and the tear of the parenchymal blood vessels to the intracerebral hematomas [
60,
79]. Microhemorrhages, mainly localized in subcortical regions of frontal, parietal and temporal lobes, have been seen in the brain of individuals exposed to blast [
80,
81]. A traumatic cerebral vasospasm with distinct temporal profile has been described in patients after blast exposure: it can develop early, often within 48 h of injury and can also present later, typically 10 or more days after initial injury [
82]. Usually, traumatic cerebral vasospasm is mainly stimulated by SAH. Nevertheless, a recent experimental study implied that SAH is not necessary for shock wave induced vasospasm [
83].
It has been suggested that the propagation of the shock wave through the vasculature represents a single rapid mechanical insult to the blood vessels’ lining (endothelium and vascular smooth muscle); it induces hypercontractility and remodeling, indicative of vasospasm initiation [
84,
85].
[...]
Response mechanisms triggered by the ANS
The pressure wave’s propagation through the body increases the pressure
inside organs [
30].
In the lungs, such a pressure increase causes instantaneous pulmonary hyperinflation and stretches the alveolar walls [
47,
94]. This, in turn, stimulates the juxtacapillary J-receptors located in the alveolar interstitium and innervated by vagal fibers [
95]. The subsequent vago–vagal reflex causes rapid shallow breathing, bradycardia and hypotension, which all are frequently experienced symptoms immediately after blast exposure. In addition, pressure receptors in the wall and trabeculae of the underfilled left ventricle may activate the C-fiber afferent nerves resulting in paradoxical bradycardia, which in turn decreases the contractility of myocardium and deepens arterial hypotension. This cardiovascular decompressor (so-called Bezold–Jarisch reflex) [
96] could further contribute to cerebral hypoxia [
94,
97] and significantly contribute to the pathobiology of BINT.
Now it gets to the carotid artery and how quickly it happens.
Consequences of increased vascular load
Experimental studies showed an early pressure surge through both arterial and venous vasculatures caused by the coupling of the shock wave with the body. In a series of experiments using pigs fitted with armor (i.e., lead- and foam-lined vest that covered the torso), individual printed circuit board piezoelectronic transducers were implanted in the inferior vena cava (IVC), common carotid artery (CCA), forebrain, thalamus, lateral ventricle and hindbrain of the hemisphere ipsilateral to the blast and in the thalamus of the contralateral hemisphere [
98]. The major peaks in the CCA
were seen 2 ms after blast, followed by a gradually increasing pressure in the IVC
that reached the peak at about 4–5 ms after the first and largest peak pressure within the CCA. Interestingly, the major pressure peaks measured by intraparenchymal and ventricular printed circuit boards occurred later,
between 136 and 138 ms after blast. The authors hypothesized that both vascular (CCA and IVC) pressure responses
might be caused by myocardial compression. The slight difference between them could be resulting from the different lengths of the CCA–heart and IVC–heart paths, respectively. Since the path into the CCA is shorter from the heart,
the rise might be more immediate [
98].
This early pressure surge t
hrough both arterial and venous vasculatures and the resulting fluid sheer stress might increase the platelet-activating factor induced neutrophil activation [99] and intensify the release of other mediators/modulators originating from endothelial cells [
100,
101], which in turn might contribute
to the early [102] and cyclic opening of the blood–brain barrier after BINT.
Not being versed in these matters, it does seem that the inner body immediatly does a lot of things in the presents of a shock wave.
