- SNIP -
Dr. Burisch Elaborates On
2 Types Of ET Physiology
From Bill Hamilton
skywatcher22@hotmail.com
4-23-5
Dan has answered the questions concerning the apparent disparity in the description of J-Rod and has been allowed access to the briefing documents to quote from as well as give his own experiences in analyzing the J-Rod (ET) housed in the clean-sphere at S-4-5 (fifth level).
Here is Dan's response received today April 23rd, 2005.
Bill -
I have received information of excellent provenance that provides a definitive answer which lies between your two points of resolution. I am quite surprised that such was offered, as the source understood I would be responding to your query. (Oh, well! Bully for us!) I was provided with this information (#Q-91-740King), during one of my briefings, but didn,t pay as much attention to it when first provided it, as I was more interested in the biological considerations. I remember skimming it, but the societal stuff wasn,t my "thing." (If you recall, I advised you of that fact, during one of our early meetings at UNLV.) Being that I was already exposed to the document, I had permission within my emeritus status to have it read to me under the understanding that it was for the purpose of refreshing my memory.
The J-Rod at LANL (no longer alive) was a separate J-Rod that arrived in a cooperative effort with the S4 J-Rod. The LANL J-Rod was resident at P+45k-yr. (rounded) at Reticulum, whereas the S4 J-Rod was resident at P+52k-yr. (rounded) at Gliese. The LANL J-Rod was sent to combine efforts with his future (a future exchange effort between societies), with the S4 J-Rod stationed at Gliese. Both traveled to the P-52y location in the Arizona desert as a combined scientific emissary team, which was supposed to land in New Mexico and be greeted by representatives of the MJ-12 working group. The report reads that the crash occurred near Kingman, Arizona. The report makes allusion to a third EBE, dead at the impact site. It makes no other declaration about it. I know it was supposed to be a briefing, but the report was written more in the style of a filed report, and contained areas of both detailed and less tightly woven information.
The report goes on to indicate that the P+52k-yr J-Rods (hereafter called 52's) who have been assigned to Gliese are those suffering from higher rates of the peripheral neuropathy as they are no good to the society from whence they came. The higher ambient partial pressure of hydrogen and lower normal environmental temperatures enable them to carry out their societal functions, as those conditions reduce symptoms of the neuropathy. The 52's society is such that a strict utilitarian approach is maintained over its individuals. This was a way to make them "worth their salt", from their leader,s perspective. The P+45k-yr. J-Rods (hereafter called 45's) are those scientific representatives, direct from Reticulum, not suffering from active peripheral neuropathy.
Both representatives possess the generalized short, slim, stature. This report indicates the 52's to possess the Type-1-Cockayne- Syndrome-like appearance, and range between 0.91m-1.07m in height (normal stance). The 45's stand more erect, and appear significantly taller as a result (normal stance: 1.07m-1.22m). (These numbers must supercede any other recollections of mine as they come right from the measurements in the briefing dossier.) There are also anatomical differences, such as variants in cranial protuberances, eye size, and such...but that is not germane to the issue at hand.
The 45's are accustomed to breathing approximately 18% ambient oxygen, whereas the 52's are able to acclimate to that same level when the neuropathy is not exacerbated, with supplemental hydrogen partial pressures being therapeutic (see reason below). The report clearly indicates that hyperbaric therapy was applied to both the 45 and the 52, with the 45 recovering sufficiently to handle the present day atmosphere, and the 52 existing likewise (with intermittent supplemental hyperbaric therapy) until August, 1991. The report doesn,t specify when the J-Rod was consigned to permanent enclosure, but it is clear that he could sustain himself in our atmosphere, for short periods, as close as a few years prior to my interaction with him.
During the time of first introduction to the 52, it was clear that he could not sustain himself outside of the pressurized clean-sphere environment. True enough, by then he could not. In fact, atmospheric variations were used to control the 52's behavior, through the use of negative reinforcement, by pressure induced intumescence. (I was never involved in that kind of activity.)
This briefing dossier also included societal and political perspectives. Prior to my involvement, his formal status changed from "guest" to "prisoner" as there existed a schism between the human authorities and the society of 45's, then showing an upwelling of political activity by the "rogues." The 52 was held under arrest, for that reason, as the suspicion was transferred to their society. The "rogues", resident at the time of the 45's, didn,t have representation from the 52's society. That caused the human authorities to suspect that the "rogues" were actually in charge of the 52's society and were therefore cloaked under the guise of the majority and not separated as a distinct minority group.
As I understand it, the "rogues" in their attempts to justify themselves, are also attempting to change the timelines such that they do not become socially extinct within 7 thousand years between 45 and 52 societies. It may be useful to reiterate that should a cataclysm occur in concert with the history books of the J-Rods, that the evolutionary process which ultimately results in the production of the J-Rods and the Brothers from Orion occurs over many thousands of years of evolutionary process. (i.e. It doesn,t happen overnight!) The only thing we would see, during our lifetime, would be the dead and the efforts to survive on the surface and in the subterranean areas and facilities. Any divergence occurs hundreds of generations into the future. I do believe, in my heart, that we will avert the catastrophe, that the timelines will collapse, and that "something wonderful" will either happen or begin to happen.
(Regressing to the mean {so to speak}, though: Implicit in that is also the recognition of prophecy and tribulation. Again, no free lunch, by why would we ever expect it? Just a note - why do the carnival barkers in the media refuse to present that statement/position of mine: looking to a successful future for humanity? They consistently paint the doom then declare themselves as positive, when the only thing they are positive on is their own financial status and fleeting fame. Is it just that they are that desperate to feel in charge, or gain some distorted view of leadership? Sad...anyway...)
Now, on to my direct experiences and the linkage between them and the information contained in the briefing.
I will try to confine my comments to his self perception, the issues regarding the neuropathy and heat loss, and the extraterrestrial cytology germane to the discussion; in reverse order.
General cytology as germane to this discussion: (from personal recall, not the report.)
In early discussions, I referred to the general cytology of the 52's as possessing an "external" and "internal" cytoplasm. Not much was made of it, during any previous interview, and from my standpoint I was always confounded by that lack of inquiry. Of course, I am looking at it from a single direction and am biased toward the biological attributes surrounding my experiences.
The discrete cytoplasmic partitioning was at the focus of the initial investigation, and the team previous to one to which I was assigned left the possible evolutionary pathway leading up to that partitioning as their greatest unsolved mystery. Once we finally received a thorough briefing, we took that issue up and carefully conducted our own investigation into the EBE,s cytology. Of course we used the previous team's reports, presumptive physiology, biochemistry, photomicrography and electron micrographs to frame up the strategy for understanding the functional morphology. We found that the previous team had rushed through the description of the "median cytoplasmic membrane" (that membrane separating the internal and external cytoplasm).
That median membrane was found to be composed of an approximately 58 angstrom thick active smooth endoplasmic reticulum (sER) with an ultrastructure demonstrating multiple vesicular pockets, with probable function of membrane phospholipid synthesis. Some anomalous 20-30 angstrom vesicles were observed, on the exterior (toward outer cytoplasmic membrane) and interior (toward nucleus) surfaces. Those vesicles were associated with what was later determined to be probable endosymbiotic nanobacteria. Ribosomes were ruled out. Rough ER (rER) was found associated with the sER, but that function moves away from the focus of this discussion. Further vesicles were found to be fused to mitochondrial analogs, on exterior and interior surfaces.
The mitochondrial analogs were of two varieties: ones that operated under probable prosaic terrestrial oxidative phosphorylation (internal, toward nucleus) and a unique bioregulatory solenoid-like process (external, toward outer cell membrane). The external variety contained cristae, but also invaginated packets which encased the cristae and acted as hydrogen sensors via an anomalous "gated" diffusion barrier. Yes, the mitochondrial- analog,s genomes (external and internal varieties) were sequenced and we positively identified selector genes, sequences probable for conservation of nuclear-to-mitochondrial redundancy, and potential enhancer modules. All this data also reinforces the wonderful work of Margulis, relevant to S.E.T.: in other words, the exterior mitochondrial-analogs are presumed to be former endosymbiotically maintained extraterrestrial microbes, probable origin- Reticulum.
So, now you are bored and are asking yourself, "Where is all this going?"
The external cytoplasm acts to increase the available energy, when higher amounts of hydrogen are present and when the temperature of the system is lowered, and supplants the internal cytoplasm,s functions during times of stress to normal cellular equilibrium. Initially, we were limited to the estimation of the equilibrium constants via van,t Hoff (as like the standard log(k1/k2=DHo(T2-T1)/2.303...RT1T2), but were able to nail down the equilibrium pressures across the cell,s exterior plasmalemma and median membrane. (This was specifically alluded to / referred to in the Q94, dealing with action potential generating cells. Of course, by the time the Q94 was produced, we had been specifically targeting the focus of the pathology, whereas much of this is general EBE cellular physiology.)
Now, as you may have learned in a college level biology course, differentiated cells, comprising specific tissues, conduct specific activities that are defined as that tissue's "function." For instance, cells of a tissue that produce...say...a large amount of a specific type of an anti-freeze glycoprotein (AFGP), would possess the appropriate complement of cellular apparatus (number/ratio of appropriate organelles, etc.) to complete the assemblage, packaging, distribution, and exporting of that protein.
Armed with this knowledge, we can now turn to the usage of AFGPs by the 52s. Without going into hours of anatomical descriptions of locations and orientations, suffice to say (for now) that exocrine and paracrine glands exist for the production of specific AFGPs which act toward thermal hysteresis. We positively identified two varieties of AFGPs: conventional Type 1s (Thr-Ala-Ala) which formed alpha-helical secondary structures and Type 3s containing the parallel/antiparallel beta-sheets.
As temperature was decreased around the 52 variety J-Rod, AFGPs were specifically produced as a physiological result, via increased signaling ultimately into the internal cytoplasm's apparatus. This function was carried out via a merocrine-like methodology. Peripheral neuropathy decreased the signaling to the glands, and life-threatening hypothermia resulted!
On transition from the S4-5's Suite Level to the S4-4's Gallery Level (where I worked in the clean sphere), the temperature was specifically reduced and hydrogen partial pressures altered, in trials, so as to determine trigger points and baselines (dependent on the neural tissue,s removal point and level of pathogenesis), thus enabling us to create a "functional" gross anatomical map of the disease progression. We applied this data against morphometric magnetic resonance type imaging, then staffed it (along with the neurochemistry, associated biochemistry, and histopathology results) against known neuro-biological theory and defined neuropathologies.
We found a completely alien (no surprise there) combination MGUS (with specific paraproteins) and anomalous CIDP-like (IgA involved) neuropathy. Immunotherapy was applied via multiple techniques, including t-cell immunosuppression, plasma exchange, blah, blah, blah! Later, even viral transfections were applied. Nothing we applied provided more than minimal and short-lived amelioration of symptoms! Further, the Cockayne-like syndrome increased (by magnitude) the difficulty in handling the pathology, and turned the issue into an almost unimaginable multifocal process.
An extensive attempt to further delineate the cytochemistry was applied, and I gradually headed-up the process to apply an early precursor study, using a reversine-like cyclohexylaminopurine. We attempted to dedifferentiate the EBE neuroblasts (by this process and by using mechanical teasing with subsequent chemical/electrical stimulation), with little usable success. As the process of some protein tertiary structure alteration progressed, a sloughing off of the external cytoplasm occurred.
- END SNIP -
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