Editing Q-94-109A/Documents/Q-94-109A

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{| class="wikitable" style="background-color:#f9f9f9; border: 1px solid #ccc; width: 100%;"
|-
! style="text-align: left;" | Document
| [[Q-94-109A]]
|-
! style="text-align: left;" | Source(s)
| https://projectcamelot.org/Q94.pdf, https://www.stealthskater.com/Documents/Burisch_3.pdf
|-
! style="text-align: left;" | Date
| 1994
|}

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<center><u>DOCUMENT NUMBER</u></center>
<center>Q-94-109A</center>

<center><u>STATUS</u></center>  

<center><u>THIS DOCUMENT IS CLASSIFIED COSMIC-<b>MAGIC</b> UNDER AUTHORITY OF TOP SECRET EXECUTIVE DECISION 91-1812-4A</u></center>  

<center><u>CLEARANCE</u></center>  

<center><b>MAGIC</b></center>  

<center><u>AUTHORITY</u></center>  

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]].  

<center><u>RELEVANT SCOPE</u></center>

This document is routed to the appropriate <b>[[MAGIC (classification)|MAGIC]]</b>-level directorate authorities of the [[Naval Space Command]], pursuant to [[Outer Space Treaty (UNOST)|UNOST]] (adopted 19 December 1965; enforced 10 October 1967). The final routing has been approved to [[Razor Back (code name)|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|Principal Investigator]], Working Group Leader (R-4800, Occupant [[Papoose Lake|Papoose]] [[S-4|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. [[Mike McConnell (U.S. Naval officer)|J. McConnell]]. (U.S.N., N.S.A., [[Majestic 12|MJ]]-[[Cosmic (classification level)|Cosmic]]) for disbursement.  

<center><u>ORDER</u></center>  

Directed by the [[Naval Research Laboratory|N.R.L.]]: "Determine, to scientific certainty, the reasons for in vivo [[neuron|neuronal]] repair failure, at [[dendrite|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 [[nerve regeneration|regeneration]]."

<center><u>SPECIFIC SCOPE</u></center>  

This results of in vitro experimentation under NSANSC directed [[Project Aquarius]] (Subintegument Neuronal Aspirative Avulsion Sampling Subsection King-24 {K-24}, [[extraterrestrial being|Extraterrestrial]] Biological Entity {[[extraterrestrial biological entity|EBE]]} A.K. [[Chi'el'ah|"AQ-J-Rod"]] {JR}) are herein related.  

<center><u>COURSE OF ACTION</u></center>  

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. [[Universal Time|U.T.]]) to Wednesday, 25 September 1996 (00:00 hrs. U.T.) 275 individual aspirative (16mm x 4mm, 0.042[[micro|μ]][[Pascal (unit)|Psc]] pressurized stick) samples were removed (at [[Pressurized Clean Sphere|C/Sphere]] [[Standard temperature and pressure|S.T.P.]]) from the right upper-appendage of [[Chi'el'ah|JR]], 6.500 cm to 6.850 cm dorsocentral to the [[medial inspirator longus]]-analog musculature, located 1.610mm into (adducted) the sinuous [[musculo-spiral]]-to-posterior [[interosseous]]-analog neuronal supraflexure, and 1.500cm (abducted) along the median [[supinator brevis]]-analog. Such methodology required the introduction of the [[Dan Burisch|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/PROPAGATION: [[Cell culture|Cell-Tissue-Culture]] (C.T.C.) Teams were deployed to plate and propagate biopsy material, under direction of [[Jonathan Fisher (Naval Research Laboratory)|Cpt. Jonathan Fisher]], M.D., Ph.D. ([[United States Navy|U.S.N.]], [[Naval Research Laboratory|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 [[Dictyostelium|dictostelium]]-desoxycholate agar media, racemic to 10.000/100.000 (%) [[glucose]]-[[acetate]] medium produced the highest cellular, fibrillar, growth rates (1.000 generations per 26.302 days). Nominal contamination-restriction protocols were followed (see: Cross contamination protocol 6, N.R.L., Document Number Q-93-016B, for procedural guidelines).

VIEWABLE PREPARATIONS: Cellular preparations were presented by the "E.B.E.-Cross-Contamination 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 Number Q-94-109B.

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

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

<center><u>CONCLUSIONS/INTERPRETATIONS</u></center>

As the conclusions, herein given, are directly interrelated with Document Numbers Q-94-109B to Q-94-109D, inclusive, the writer suggests that each be viewed <i>in toto</i>. The previous analysis (<u>k(lower-case)</u>-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 little more information than the basic [[cellular morphology]], [[organelle]] analogs, [[membrane]] communication patterns, and pathways of [[cellular constituent biosynthesis]]. Study K(upper-case)-24 was deemed necessary, by the [[authority structure]], for the purpose of handling aspirations of a fresher nature, whose <i>in situ</i> 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 possible 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 [[phenotype|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 <u>certain</u> methods to alter the present genotype should not be carried out. This position of conviction is held for [[moral]] and [[bioethics|bio-ethical]] considerations, as such actions may deter from the normal process of [[natural selection]] in the [[human species]].

Initial observations of [[exobiology|extraterrestrial]] [[microglia]]-like-analog neuro<u>blasts</u> {?}([[microglia-like extraterrestrial neuroblast|MENB's]]) revealed an approximated morphology to all such extraterrestrial cells, that being [[hypotrophism|hypotrophic]] [[perikaryons]] (as opposed to terrestrial counterparts), with a [[multipolar neuron|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 anastomosed to [[Nissl substance|nissl-like bodies]], extending afferently from the [[nuclear material]], through the internal cytoplasm, then further cementing to the exterior of the internal cytoplasm (the "ground substance" of the external 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 [[cell culture|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 [[myoneural junction]] regions, with a near 1-to-1 correspondence. Histologically, each myoneural junction viewed, demonstrated excessive filament depletion at the nominal [[axolemma|axolemmal]] ridges, with high concentrations of [[Mitochondrion|mitochondrial]]-[[Golgi apparatus|golgi]]-analog(s) (MG) at/near each synaptic trough's [[basal lamina|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 [[cell membrane|membrane]] activity was conducted, via [[freeze fracture electron microscopy|freeze fractures]] ([[Scanning Tunneling Microscope|STM]]), [[separative biochemistry]] (UCFG/MOA/MP), and selective [[histopathology|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 determined as part of the pathological process. External membrane structure showed [[ion channel]]ing at less concentrations, where the [[myoneural junction|myoneural junctions]] met the above criteria for pathology. Present channel varieties were bordered by long chain (via MP/HPLC/GC/MS) [[glycoproteins]] [IgA equivalent at [[IUPAC]] tertiary top chain representation- NeuAc(α2-6)...]., later coded (via [[gel electrophoresis]] and [[Polymerase chain reaction|PCR]]) specifically to expressions from the [[Major Histocompatibility 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 [[desmosome|protodesmosomes]] from the fibroblast-analogs communicated to the sides of the subneural cleft areas. That fibroblast-protodesmosomal-analog association has not been entirely explained.

It appears that the [[protonation|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 computed (via MP) in order to verify the mode of regulation, the results of which demonstrated that the cristae-compartmentalized [[electron transport chain|electron transport system]] ([[bioregulatory parallel capacitors]]), operated in a triad of spherical cristae, generating and temporarily preserving at 7.100 X 10exp(-12)µL per cycle. This was accomplished by reflux of hydrogen, via the MG-associated [[Phosphoenolpyruvate]] [[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|solenoid]]). The minimal output of this system (passive exothermic emission), within the [[cellular matrix]] under study, enabled [[G-protein]]s to modulate [[voltage-gated calcium channel]]s, 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 [[synapse]]s (following complete disruption of the excitatory potential, at -75mV, and with [[potassium|K+]] efflux), through progressive acidosis, secondary to the PEP-analog's output. This was the agent of [[neuropathology|neuropathogenicity]]. Correlating to increasing age, from an interview with [[Chi'el'ah|JR]] (Sigma authorized), higher rates of [[neuropathy]] are found. Additionally, [[gene mapping]] has postulated a correlation in the age-dependent expression of the IgA equivalent to the organism-wide efficiency of [[receptor tyrosine kinase]]s (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]] for sequential [[plasmid]] recombinations via [[electroporation]]. Sequential addition of expression loci for pp44superscript([[MAPK|mapk]]/[[ERK2|erk2]]) yielded a theorized alternate pathway, via pp70superscript([[S6K]]) kinase, to translational control through [[ribosomal protein S6|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 to 100 sq. mm resolution). Under order from the investigator’s [[Commanding Officer]], [[transgenic]] inocula, resulting from [[liposomal fusion]]s, 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 “[[human hybrid|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.

_____________________________________________________________

[[Dan Burisch|Danny Benjamin Crain]], Ph.D. (Captain, [[United States Navy]], N.R.L.)
Working Goup Leader, [[Project Aquarius]], R-4800, Papoose Site 4

Dictated to:

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