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{{I'm not sure what these are all about. First is an OCR copy of a telefax memo from decades ago. Second document looks like part of a research project, but I can't find an exact date associated with the file.}}

PINEHEARST COMPANY

26877 Century Drive

Fort Lee, NJ 07605
 

March 17, 1988

______________

Mr. Varlane,

Allow me to introduce myself. My name is Arthur Petrelli, Operations Director of the Pinehearst Company. We are a leading biotechnology corporation based out of Fort Lee, New Jersey. I was saddened to hear of your son Magnes' passing, I have also become aware of the personal fortune you have spent on medical equipment to research his illness and prolong his life. I believe that you and I share a common love for our families and would do anything to keep our children safe from harm. To that end, I would like to invite you to come to our New Jersey office to discuss the future of your family and what the Pinehearst Company can do for you.

With sincerest condolences,

Arthur Petrelli

Operations Director

_________________________________________________________________________________________________________________________

project-hydra_transfer_2-part3.pdf

It is generally accepted that long-term memory (LTM) is encoded as alterations in synaptic strength. An alternative model, however, proposes that LTM is encoded by epigenetic changes. Non-coding RNAs can mediate epigenetic modifications. Therefore, RNA from a trained animal might be capable of producing learning-like behavioral change in an untrained animal. Here, it is demonstrated that the memory for long-term sensitization in the marine mollusk Aplysia can be successfully transferred by injecting RNA from sensitized into naïve animals. Moreover, a specific cellular alteration that underlies sensitization in Aplysia, sensory neuron hyperexcitability, can be reproduced by exposing sensory neurons in vitro to RNA from trained animals. The results provide support for a nonsynaptic, epigenetic model of memory storage in Aplysia.

To prepare a single RNA injection, the pleural-pedal and abdominal ganglia was removed from Subject A. The total RNA was then extracted from the dissected ganglia. The ganglia were initially homogenized in Trizol reagent for 30 s; typically, 1 ml Trizol was used to homogenize the central ganglia. For every 1 ml Trizol reagent, 200 μl chloroform was added and mixed by vortexing for 15 s. After incubation at room temperature for 5-10 min, the sample was centrifuged at 12,000g for 15 min. The upper aqueous phase was transferred into a new tube. The sample was then centrifuged for 10 min at 4o C after addition of 500 μl isopropanol to precipitate the RNA. The resulted RNA pellets were washed with 70% ethanol and centrifuged for 2 min at 4o C. After being air-dried for 10 min, the RNA pellet from each tube was dissolved in 30 μl DIH2O; then the RNA from ganglia dissected from Subject A was combined into a single tube, and the RNA concentration was measured using Nano Drop (Thermo fisher ND-1000). After the RNA concentration had been determined, 70 μg of the combined RNA was aliquoted and ASW was added to this aliquot to attain a volume of 100 μl; this solution was then injected into the hemocoel of Subject B via his neck. Each recipient therefore received 70 μg of either RNA from Subject A or RNA from control clones. The DNA methyltransferase (DNMT) inhibitor RG108 (Sigma, St Louis, MO) was dissolved in DMSO to a concentration of 25 mM. To inhibit DNMT, a volume of 100 μl per 100 g of body weight of RG108 was injected intrahemocoelically into each clone.

Following the initial electrophysiological measurements on Day 1, the recording medium was washed out with normal cell culture medium. The cultures were then randomly assigned to treatment with RNA from Subject A (Trained RNA group), RNA from untrained clones (Control RNA group), or vehicle. For the RNA treatments, 1 μg of RNA was added to each cell culture dish, yielding a concentration of 0.5 μg of RNA per 1 mL of cell culture medium. The RNA from Subject A, the RNA from the control clones, or the vehicle was added to the cell culture dish and left in the dish for 24 h, after which it was washed out with the recording medium for 30 min, and the posttest electrophysiological measurements made.

Final Findings:

Injection of RNA from Subject A causes manifestation of LTM expression in recipients. To generate the RNA used for memory transfer, individual clones were given regression therapy and memory induction from trained telepathic source (Fig. 1A). The training produced clear long-term memory recovery (LTM). Immediately after the 48-h posttest, RNA was extracted from the central nervous system (pleural, pedal and abdominal ganglia) of Control and Subject A. The extracted RNA was then injected intrahemocoelically into other naïve clones (recipient; Fig. 1C). (Note that occasional groups of clones did not sensitize. The behavioral data from these replications were excluded from the analysis, and RNA was not extracted from them.) With proper training this process could be replicated native by Subject A's biological father, allowing for epigenetic memory transference from Subject A to clones without the need for practical methodology.

Complications arise in the stabilization of original non-human ability, but we are recommending transference of memory-enhanced clones to Icarus research team for synthetic enhancement.

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