These results of an in vitro experimentation under NSA/NSC directed Project Aquarius (Subintegument Neuronal Aspirative Avulsion Sampling Subsection King-24 (K-24), Extraterrestrial Biological Entity (EBE) A.K. "AQ-J-Rod" (JR) are herein related.

    Eaglesdisobey.com

    archived as http://www.stealthskater.com/Documents/Burisch_3.doc

    more of Dan Burisch is at http://www.stealthskater.com/Burisch.htm

     

note: because important web-sites are frequently "here today but gone
tomorrow", the following was archived from
http://www.skywatch-research.org/Q94-109A.htm (also at
http://www.eaglesdisobey.com/Q94%20onramp.htm ) on November 13, 2002 .
This is NOT an attempt to divert readers from the aforementioned
web-site. Indeed, the reader should only read this back-up copy if it
cannot be found at the original author's site.

 

The Q94-109A Document authored by Dr. Dan Burisch aka Dan Crain

 

This 2nd draft of a document was written in 1994 by Dr. Dan Crain at
Papoose Mountain, R-4800, Site 4 in Nevada. It has no security markings.
The original had the logo of the U.S. Naval Space Command on the first
page.

The microbiological terms in this paper have been found to be consistent
with standard use with the proviso that it refers to the alleged tissue
sampling of an extraterrestrial biological entity with a different
physiology and cell structure. This entity was known as J-ROD (and other
nicknames), a class of Grey from Gliese 876C*, a staging area for this
entity who originated in the Zeta Reticuli binary star system. This
entity was housed in an environmental clean sphere in an underground
biological laboratory at S4.

The first and last pages of the original are at
http://www.skywatch-research.org/Q94-109A.htm .

 

*Gliese 876C: The planet in this system is the only one I have been given
information about. It is not what we would consider habitable, however it
is the location that they selected for their remote staging base, the one
that they use in a cooperative effort to study and interact with us. It
was described to me as being below the cloudy surface layer, as this
planet appears to have a great deal of gas on the surface.

The rationale behind this is that both Zeta Reticuli and Sirius/Orion
were too far to keep going back to. They needed to conserve energy and
time so they established a cooperative base. When they need to return
home, they use the Gliese876C as a jump gate back to their respective
systems. Dan indicates that the light from these jumps shows up as
variability around the star but due to the distances involved (15.3 light
years from here to Gliese) that variability would not be visible here at
the same time as the jumps took place. There would be a gap time we would
have to consider.

Note from B.J. Wolf

 

Astronomical info on Gliese 876C:
http://www.extrasolar.net/star.asp?starid=2

More on Zeta Reticuli:
http://www.ufoconspiracy.com/reports/zetareticuli_star_sys.htm

 

DOCUMENT NUMBER

Q-94-109-A

STATUS

THIS DOCUMENT IS CLASSIFIED COSMIC-MAGIC UNDER AUTHORITY OF TOP SECRET

EXECUTIVE DECISION 91-1812-4A

CLEARANCE

MAGIC

AUTHORITY

Written under authorization from the Government of the UNITED STATES OF
AMERICA,

DEPARTMENT OF DEFENSE, DEPARTMENT OF THE NAVY, Naval Intelligence

Command/Naval Space Command

RELEVANT SCOPE

This document is routed to the appropriate MAGIC-level directorate of the
Naval Space Command, pursuant to UNOST (adopted 19 December 1966,
enforced 10 October 1967). The final routing has been approved to Razor
Back, by direction of 92-NSC-117. The contents of this document are to be
regarded as a final report (spec K-24) of the Principal Investigator,
Working Group Leader (R-4800, Occupant Papoose Site 4), as determined by
his Commanding Officer, Cmd. John Anthony McGuinness, M.D. (U.S.N.,
N.S.A.), under final routing to R. Adm. J. McConnell (U.S.N., N.S.A.,
MJ-Cosmic) for disbursement.

ORDER

Directed by the N.R.L.: "Determine, to scientific certainty, the reasons
for in vivo neuronal repair failure, at dendritic terminal ends, from a
set of cellular samples, in vitro. Classify such reasons, functionally,
to ascertain the mechanisms of such failure, then isolate the most
probable pre-existing cellular conditions giving allowance to proper
regeneration."

SPECIFIC SCOPE

These results of an in vitro experimentation under NSA/NSC directed
Project Aquarius (Subintegument Neuronal Aspirative Avulsion Sampling
Subsection King-24 (K-24), Extraterrestrial Biological Entity (EBE) A.K.
"AQ-J-Rod" (JR) are herein related.

COURSE OF ACTION

GENERAL: As cellular reclassification was necessary, dated by previous
testing of culture material from an "^ unknown origin^", the following
methodology was employed. From Tuesday, 19 July 1994 (22:00 hrs. U.T.) to
Wednesday, 25 September 1996 (00:00 hrs. U.T.) 275 individual aspirative
(16mmx 4 mm, 0.042PSC pressurized stick) samples were removed (at
C/Sphere S.T.P.) from the right upper-appendage of JR, 6.500 cm to 6.850
cm dorsocentral to the medial supinator longus-analog musculature,
located 1.610 mm into (adducted) the sinuous musculo-spiral-to-posterior
interosseous-analog neuronal superflecture, and 1.500 cm (abducted) along
the median supinator brevis-analog. Such methodology required the
introduction of the Principal Investigator into the Pressurized Clean
Sphere, which constituted an I.G.A.-declared "Extraterrestrial Close
Encounter (E.C.E.), Class IV c". Protocols for the debriefing of the
Principal Investigator were followed (Document Number unknown to the
writer). Resultant samples were imaged, labeled, and transferred to
C/Sphere S.T.P. elation tubes for analysis.

INITIAL SAMPLE STABILIZATION/PROPOGATION. Cell-Tissue-Culture (C.T.C.)
Teams were to plate and propagate biopsy material, under direction of
Cpt. Jonathan Fisher, M.D. , Ph.D. (U.S.N., N.R.L.). The subdivided
samples (1-100 per each stick) were designated as K-24-1 through
K-24-100, respectively. Each fraction, specialized analysis, were given
subsplit labels K-24-1-a,b,c,^ "n" through K-24-100-a-b-c,.. "n",
respectively. The plating activities were entirely successful at C/Sphere
S.T.P., save K-24-16, K-24-36, and K-24-81. Heightened osmotic pressure
from excess colloidal suspension was interpreted as the reason for
cellular stasis and death. Equal combinations of pressurized
dictostelium-desoxycholate agar media, racemic to 10.000/100.000(%)
glucose-acetate medium produced the highest cellular, fibrilar, growth
rates (1.000 generations per 26.302 days). Normal
contamination-restriction protocols were followed (see: Cross
contamination protocol 6, N.R.L., Document Number Q-93-0168 , for
procedural guidelines).

VIEWABLE PREPARATIONS: Cellular preparations were presented by the
"E.B.E.-Cross-Contaminations and Viewing Protocols (Sections 1-4)", as
approved 2 April 1993 (N.R.L., Papoose Site 4, Document Number
Q-93-016C.)

CELLULAR SUBFRACTION ANALYSIS: See Document Q-94-109B.

AMBIENT BIOCHEMISTRY: See Document Number Q-94-109C.

SUBFRACTION BIOCHEMISTRY: See Document Number Q-94-109D.

CONCLUSIONS/INTERPRETATIONS

As the conclusions, herein given, are directly interrelated with Document
Q-94-109B to Q-94-109D, inclusive, the writer suggests that each be
viewed in toto. The previous analysis (k(lower-case)-24), of then "^
cells of an unknown origin^" yielded presumptive declarations that such
specimens were operating under different methodologies than known
terrestrial counterparts. That study also attempted the same process of
"back-engineering" the cellular constituents, but yielded more
information than the basic cellular morphology, organelle analogs,
membrane communication patterns, and pathways of cellular constituent
hypothesis. Study K(upper-case)-24 was deemed necessary, by the authority
structure, for the purpose of handling aspirations of a fresher nature,
whose in situ value would be known, and wherein a clear purpose to the
investigation would be open to the operating group under the writer's
control. The order was interpreted, clearly, as a study in the
classification of neuronal dendritic repair failure, the establishment of
the probable mechanisms of such failure, and the ascertaining of probable
previous conditions (conditions that would necessarily have been present
for acceptable evolution) when such repairs would have been successful.
Additionally, the operating group took the opportunity to
"back-engineer", together with theoretical applications, a potential
route of ultimate repair of the dysfunctional system.

This report declares that the present operating group fulfilled the
aforementioned order, and was also successful in positing the most likely
route of genotype repair, a pathway completely reparative to the present
phenotypic status. While the writer must present the findings, it must
also be stated that the operating group members have made a unanimous
declaration that certain methods to alter the present genotype should not
be carried out. This position of conviction is held for moral and
bio-ethical considerations, as such actions may deter from the normal
process of natural selection in the human species.

Initial observations of extraterrestrial microglial-like-analog
neuroblasts(?) (MENB's) revealed an approximated morphology to all such
extraterrestrial cells, that being hypotrophic perikaryons (as opposed to
terrestrial counterparts), with a multipolar-type generalization. The
presence of an external and internal cytoplasm, specifically herein
defined as the neuroplasm (as previously described in k(lower-case)-24),
was again presented, with the organelle fusion being also demonstrated.
The neurofibrils were present, with a 1-to-1 terrestrial relationship of
neuroprotofibrils (c. 0.009 mm). It occurred to the investigator that the
neuroprotofibrils were selectively anastomosed to nissl-like bodies,
extending afferently from the nuclear material, through the internal
cytoplasm, then further cementing to the exterior of the interior
cytoplasm (the "ground substance" of the exterior cytoplasm); however,
such processes continued along primary axon units, but terminated at the
primary-axonic-dendritic-process juncture (where the axoplasm
sufficiently thinned allowing branching dendritic processes). This
finding led the investigation toward its ultimate conclusions.

At the point of neuroprotofibril excision, the analog to the Incisure of
Schmidt-Lanterman, Neurokeratin-like networks, and solid Endoneurium,
cease. Cross culturing revealed that selective culture necrosis was not
the origin. Further, such early terminations were found at highest rates
(38 hits per 50 units at 25,000 diameters magnification), when adjacent
to higher numbers of fibroblast-analogs, within the endoneurium. This
correlation extended to myroneural junction regions, with a near 1-to-1
correspondence. Histologically, each myroneural junction viewed,
demonstrated excessive filament depletion at the nominal axolemmal
ridges, with high concentrations of mitchondrial-golgi-analog(s) (MG)
at/near each synaptic nerve trough's Basal Lamina, along the sides of
each subneural cleft. This demonstration drew a conclusion of a
pathological process that may associate myocyte physiology,
fibroblast-analog response and/or mediation, membrane interactions, and
axoplasm response.

A detailed analysis of membrane activity was conducted, via freeze
fractures (STM), separative biochemistry (UCFG/MOA/MO), and selective
histopathological supravital staining (LM). [*See attached coding for
machinery references.*] The results indicated that the hydrogen mediated
phosphorylation, as was presented in a Danielli model in previous
reference k(lower-case)-24, occurred at higher rates of successful energy
budgeting (5.000%, average, power) at those areas where subneural clefts
were shortest. Further, the highest concentrations of
mitochondrial-golgi-analogs were found at the shortest of such clefts.
This necessary proximity was found at each analysis, and was therefore
determine as part of the pathological process. External membrane
structure, showed ion channeling at less concentrations, where the
myoneural junctions met the above criteria for pathology. Present channel
varieties were bordered by long chain (via MP/HPLC/GC/MS) glycoproteins
[lgA equivalent at IUPAC tertiary top chain representation- NeuAca(206)
(sp?) ^], later coded (via gel electrophoresis and PCR) specifically to
expressions from the Major Histocomptability Complex (MCH) at locus
HLA-Cw3(a), and seemingly selective to those ion channels that disfavor
membrane disequilibria, thus lack of net polarity, and where
protodesmosomes from the fiberblast-analogs communicated to the sides of
the subneural cleft areas. That fibroblast-protodesmosome-analog
association has not been entirely explained.

It appears that the protonated phosphorylation complex, within the
MG-analog, operating (as best known) is rather more interwoven with
voltage gated membrane channels than previously thought. A classification
analysis was completed (via MP) in order to verify the mode of
regulation, the results of which demonstrated that the
cristae-compatmentalized electron transport system (bioregulatory
parallel capacitors), operated in a triad of spherical cristae,
generating and preserving at 7.100 x 10exp(-12)J per cycle. This was
accomplished by the reflux of hydrogen, via the MG-associated
Phospshoenylpruvate Phosphotransferase-analog (PEP-analog) active pump,
and using glucose-6-phosphate as a carrier, also found preserving energy
within the system as X = 2W / lexp(2); therefore inductance (a
bioregulatory solenoid). The minimal output of this system (passive
exothermic emission), within the cellular matrix under study, enabled
G-proteins to modulate voltage-gated calcium channels, and
simultaneously, internal ligand and kinase modulated varieties to act in
antagonism. It was the localized effect of this antagonism that
interrupted the potential sufficiently to begin collateral elimination of
synapses (following complete disruption of the excitatory potential, at
-75 mV, and with K+ efflux), through progressive acidosis, secondary to
the PEP-analog's output. This was the agent of neuropathogenicity.
Correlating to increasing age, from interview with JR (Sigma authorized),
higher rates of neuropathy are found. Additionally, gene mapping has
postulated a correlation in the age-dependent expression of the lgA
equivalent to the organism-wide efficiency of receptor tyrosine kinases
(Q-94-109C/D). From that line of evidence, repair processes were found
altered, via translational control inhibition at pp90exp(rsk)-analog.
Simply put, repair was faulted, via increasing age, by insufficient
specific protein kinase levels.

Attempts to rectify the problem, via allogenic recombination, resulted in
an allomeric response. The neuropathy continued. Human Subject #58-001
(refer to autopsy Document Q-96-029) supplied bone marrow to for
sequential plasmid recombinations via electroporation. Sequential
addition of expression loci for pp44superscript(mapk/erk2) yielded a
theorized alternate pathway, via pp70superscript(S6K) kinase, to
translational control through S6 phosphorylation. Transplantation of such
cell matrix inocula resulted in attenuation of the neuropathy, not
localized, but over a considerably wide area (2 cu. mm. inoculum t0 100
sq. mm. Resolution). Under order from the investigator's Commanding
Officer, transgenic inocula, resulting from liposomal fusions, were
attempted using secondary spermatocyte stock, with the same degree of
success; however, the mechanisms of that result remain unknown. Such
lines of investigation, with a clear "cross breeding" intent, should be
followed with the greatest concern and suggested "hesitation", as the
leakage of such success could promote a 'wild' contaminant species to
further the experimentation in an unabated fashion. The ultimate results
of such a possible genetic introduction into the human population could
be catastrophic.

This report is respectfully presented for consideration.

 

 

 

 

 

Danny Benjamin Crain, Ph.D. (Captain, United States Navy, N.R.L.)

Working Group Leader, Project Aquarius, R-4800, Papoose Site 4