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Reconsider of James Holmes

Author: Genecks
B.S. Neuroscience

These are but my opinions and speculations and to be of a measure of my character.

I’ve been considering James Holmes as of late. I believe I understand what happened to him. I’ve considered that he must have schizoaffective disorder. In that, I’m assuming he held some delusional, paranoid belief. Eventually, enough stimuli excited that delusional, paranoid belief and he had a psychotic break. Sometime after the psychotic break, he underwent dysphoric mania. From this point, he underwent a level of repression from the stimuli that were associated with and had excited his delusional, paranoid belief. After the repression occurred, he held a level of continued dysphoric mania whereby he had transference of mental contents from one part of his memory/personality to another part of his memory/personality. And then he became the Joker.

Of interest here, however, is Ribot’s law.

Behavioral epigenetics: Dissociation and repression

Something I have been wondering about as of late is the biological basis for dissociation and repression. I am an identity theorist when it comes to understanding psychological phenomena. Also, I do understand why psychology is around as a science. I, nonetheless, believe psychology is based on biological aspects of the central and peripheral nervous systems.

Of interest is dissociation and repression.

I’d like to start this with something I’ve read:

what is the difference between the two defense mechanisms Dissociation and Repression ?
Has it got to do with recent event (Dissociation) and past event (Repression) ?

A person’s reply:

This is a good question because it reminds me all the whimsical nature of USMLE tests.

Basically all about defense mechanisms is bullshit. If we had to say something useful about it, we could say they are just ways for the mind to cope with trouble. Beyond that, as far as I know, nobody has identified the Brodmann’s area in the brain where those defense mechanisms lie. Nobody, to my scant knowledge, has demonstrated any correlation with PET scans of the brain. Nobody, to my little reading, found any mutation in any gene that makes more people prone to use this or the other defense mechanism. There’s no animal model nor a drug that enhances any such mechanism.

However, these so called ‘defense mechanisms’ and their definitions do help psychiatrists make their language sophisticated. For example, blocking a painful memory (repression) or just taking the good side of it (dissociation) which in essence both are DENIAL, help psychiatrists keep their notes organized. Because they are always trying to find the neuron or the ion channel that controls either one, that’s how they can keep submitting grants, writing publications requesting more research on the topic, and we students try to memorize such capricious definitions of something that basically looks like denial. If we fail to get the right score, it’s not because such defense mechanisms are baloney, but it’s because we are repressing the fact we are poor students and don’t deserve to match.

source: (year: 2012)

Ok, first off, I have a couple of problems with the reply, regardless of the English used.

In the 2000s, behavioral epigenetics became more of a popular field of study. As such, I believe that more is to be conducted in the realm of behavioral epigenetics than before. However, the problem with behavioral epigenetics in the realm of human neurobiology is that you cannot easily grab a bunch of humans with dissociated or repressed memories and study them.

There are a few problems:

1) The individuals with repressed or dissociated memories more than likely do not know they have the amnesia
2) There are ethical problems with using humans as experimental subjects
3) If you could find individuals with repressed or dissociated memories, then I’m assuming the individual has been informed of this (they’ve been informed of a logic error).

The only way you could really get a great human subject is if you found individuals with repressed or dissociated, kept them blind to the fact that their memories are dissociated or repressed, and then experimented on them. However, that opens a whole new ethical problem: The individuals would want to know why you’re experimenting on them.

You could attempt to tell them that they have dissociated or repressed memories without telling them which or what memories, but once that occurs, the possibility for the individual to begin questioning the reality of the situation occurs. As such, the experimental data has the possibility for becoming biased.

Regardless, in a world where research scientists grab individuals with dissociated or repressed memories, they could attempt to look into the neurobiological causes of dissociated or repressed memories.

Sure, people could attempt to do MRI scans. They could lie to individuals with dissociated or repressed memories, thus hoping to get MRI scans before making the individuals aware of their memory problems.

Sure, blood work could be done. Some analysis of reflex motor control, REM cycle, and other topical studies could be done.

Beyond that, the molecular biological and electrophysiological work needed would fall into some serious ethical issues, as they would require surgery.

Regardless of having human animal studies, it would be difficult to determine whether or not a mouse or rat has dissociation or repression. I have considered that repression in mice may occur due to various condition training. I have read that when a certain experiment with stimuli is done to a mouse in a particular condition, it will give a particular response. However, when the mouse is put into a different condition (environmental setting) with the same stimuli, it will not give the response.

I believe the example was a toxin, for instance. I assume you could relay this also into drug addiction and overdoses.

With drug addicts, if they do drugs in a particular environment, they learn to develop a tolerance. However, you take the drug addict to a different condition, the tolerance will be decreased, because the condition has an influence on the tolerance, thus increasing the possibility for an overdose to occur.

As such, repression or dissociation in this situation could be analogous with the tolerance to the environment. In other words, developing a tolerance is learning to repress negative outcomes. However, in a different condition, the learned ability to repress a negative outcome is decreased, thus the ability for the negative outcome to surface is increased.

That’s a hypothesis at best, but there seems to be some similarity. And in terms of an animal model, that seems to be as close as things get.

As such, one might be able to develop a model for “love trauma” by giving a mouse drugs, which simulate love.

However, this is but speculation.

I believe there have been epigenetic studies conducted in relation to drug addiction in animal models. Loss of the drug could be considered traumatic. And if the trauma is enough, it could potentially dissociate and repress the animal. However, the thing would be finding a way to determine what the animal has dissociated from. As such, I assume an experiment where the drug is paired with a negative stimulus could eventually lead to the animal repressing/dissociating from the negative stimulus while having a desire for the drug. Dissociation or repression would be noticeable if the animal ignores or gains a tolerance to the negative stimulus. However, the methods whereby the negative stimulus occur would have to be considered. The negative stimulus could be a form of second-order conditioning. If the animal ignores the second-order negative stimulus while in the presence of it and continues to seek the drug, then the animal has dissociated, repressed, or forgotten about the second-order negative stimulus.

As such, it could be assumed that the animal has dissociated, repressed, or forgotten its memories. From this point, you could attempt to do neurobiological research on the animal for an animal model of dissociation or repression. From this point, a behavioral epigenetic relationship between dissociation and repression could be determined.

I think that might work, but it may not.

Either way, behavioral epigenetics in the realm of dissociation and repression are still starting out.

I’ve come across an article:
By: Robert Scaer, M.D.

Published in: Applied Psychophysiology and Biofeedback, (2001), 26(1), 73-91, based on a Keynote Address presented at the 31st annual meeting of the Association for Applied Psychophysiology and Biofeedback, March 29-April 2, 2000, Denver, CO.

He appears to go into some level of detail about dissociation as a neurobiological event. This is admirable. However, I do not like the animal model based on freeze events. I believe more can be done in developing animal models in relation to conditioning, trauma, stimuli, and dissociation.

Identification of candidate genes affecting delta(9)-tetrahydrocannabinol biosynthesis in Cannabis sativa

J Exp Bot. 2009;60(13):3715-26. Epub 2009 Jul 6.
Identification of candidate genes affecting Delta9-tetrahydrocannabinol biosynthesis in Cannabis sativa.

Marks MD, Tian L, Wenger JP, Omburo SN, Soto-Fuentes W, He J, Gang DR, Weiblen GD, Dixon RA.

Department of Plant Biology, University of Minnesota, St Paul, MN 55108, USA.

Abstract: RNA isolated from the glands of a delta(9)-tetrahydrocannabinolic acid (THCA)-producing strain of Cannabis sativa was used to generate a cDNA library containing over 100 000 expressed sequence tags (ESTs). Sequencing of over 2000 clones from the library resulted in the identification of over 1000 unigenes. Candidate genes for almost every step in the biochemical pathways leading from primary metabolites to THCA were identified. Quantitative PCR analysis suggested that many of the pathway genes are preferentially expressed in the glands. Hexanoyl-CoA, one of the metabolites required for THCA synthesis, could be made via either de novo fatty acids synthesis or via the breakdown of existing lipids. qPCR analysis supported the de novo pathway. Many of the ESTs encode transcription factors and two putative MYB genes were identified that were preferentially expressed in glands. Given the similarity of the Cannabis MYB genes to those in other species with known functions, these Cannabis MYBs may play roles in regulating gland development and THCA synthesis. Three candidates for the polyketide synthase (PKS) gene responsible for the first committed step in the pathway to THCA were characterized in more detail. One of these was identical to a previously reported chalcone synthase (CHS) and was found to have CHS activity. All three could use malonyl-CoA and hexanoyl-CoA as substrates, including the CHS, but reaction conditions were not identified that allowed for the production of olivetolic acid (the proposed product of the PKS activity needed for THCA synthesis). One of the PKS candidates was highly and specifically expressed in glands (relative to whole leaves) and, on the basis of these expression data, it is proposed to be the most likely PKS responsible for olivetolic acid synthesis in Cannabis glands.

I see what you did there…

I see what you did there. -_o

I see what you did there, you silly dimer alpha-beta spectrin molecule… you made a tetramer via a self-association site..

protein schematic

Protein 4.1R-dependent multiprotein complex: New insights into the structural organization of the red blood cell membrane

Protein 4.1R (4.1R) is a multifunctional component of the red cell membrane. It forms a ternary complex with actin and spectrin, which defines the nodal junctions of the membrane-skeletal network, and its attachment to the transmembrane protein glycophorin C creates a bridge between the protein network and the membrane bilayer. We now show that deletion of 4.1R in mouse red cells leads to a large diminution of actin accompanied by extensive loss of cytoskeletal lattice structure, with formation of bare areas of membrane. Whereas band 3, the preponderant transmembrane constituent, and proteins known to be associated with it are present in normal or increased amounts, glycophorin C is missing and XK, Duffy, and Rh are much reduced in the 4.1R-deficient cells. The inference that these are associated with 4.1R was borne out by the results of in vitro pull-down assays. Furthermore, whereas Western blot analysis showed normal levels of band 3 and Kell, flow cytometric analysis using an antibody against the extracellular region of band 3 or Kell revealed reduction of these two proteins, suggesting a conformational change of band 3 and Kell epitopes. Taken together, we suggest that 4.1R organizes a macromolecular complex of skeletal and transmembrane proteins at the junctional node and that perturbation of this macromolecular complex not only is responsible for the well characterized membrane instability but may also remodel the red cell surface.

Now viewing through an eye-piece:

Annual Review of Neuroscience
Vol. 32: 435-506 (Volume publication date June 2009)
Advances in Light Microscopy for Neuroscience

Brian A. Wilt, Laurie D. Burns, Eric Tatt Wei Ho, Kunal K. Ghosh, Eran A. Mukamel, and Mark J. Schnitzer
James H. Clark Center and Howard Hughes Medical Institute, Stanford University, Stanford, California 94305; email:

Since the work of Golgi and Cajal, light microscopy has remained a key tool for neuroscientists to observe cellular properties. Ongoing advances have enabled new experimental capabilities using light to inspect the nervous system across multiple spatial scales, including ultrastructural scales finer than the optical diffraction limit. Other progress permits functional imaging at faster speeds, at greater depths in brain tissue, and over larger tissue volumes than previously possible. Portable, miniaturized fluorescence microscopes now allow brain imaging in freely behaving mice. Complementary progress on animal preparations has enabled imaging in head-restrained behaving animals, as well as time-lapse microscopy studies in the brains of live subjects. Mouse genetic approaches permit mosaic and inducible fluorescence-labeling strategies, whereas intrinsic contrast mechanisms allow in vivo imaging of animals and humans without use of exogenous markers. This review surveys such advances and highlights emerging capabilities of particular interest to neuroscientists.


English Breakfast tea has the potential to inhibit the activity of anthrax, as long as the tea doesn’t contain milk, according to an article published in the March 2008 issue of Microbiologist magazine.


Now playing:

The Mother Centriole Plays an Instructive
Role in Defining Cell Geometry


Centriole positioning is a key step in establishment and propagation of cell geometry, but the mechanism of this
positioning is unknown. The ability of pre-existing centrioles to induce formation of new centrioles at a defined angle
relative to themselves suggests they may have the capacity to transmit spatial information to their daughters. Using
three-dimensional computer-aided analysis of cell morphology in Chlamydomonas, we identify six genes required for
centriole positioning relative to overall cell polarity, four of which have known sequences. We show that the distal
portion of the centriole is critical for positioning, and that the centriole positions the nucleus rather than vice versa. We
obtain evidence that the daughter centriole is unable to respond to normal positioning cues and relies on the mother
for positional information. Our results represent a clear example of ‘‘cytotaxis’’ as defined by Sonneborn, and suggest
that centrioles can play a key function in propagation of cellular geometry from one generation to the next. The genes
documented here that are required for proper centriole positioning may represent a new class of ciliary disease genes,
defects in which would be expected to cause disorganized ciliary position and impaired function.

Phage Therapy

Once in a while, I’ll end up reading about something I haven’t read in years. That’s the kind of person I am, and I tend to do that toward things I don’t have much money nor knowledge invested in. So, let’s take a look at the advances in phage therapy.

A controlled clinical trial of a therapeutic bacteriophage preparation in chronic otitis due to antibiotic-resistant Pseudomonas aeruginosa; a preliminary report of efficacy
Wright, A.*, Hawkins, C.H. † , Änggård, E.E. † & Harper, D.R. †
*UCL Ear Institute and Royal National Throat, Nose and Ear Hospital, Grays Inn Road, London , and † Biocontrol Limited, BioCity, Pennyfoot Street, Nottingham, UK
Correspondence to Anthony Wright, UCL Ear Institute and Royal National Throat, Nose and Ear Hospital, Grays Inn Road, London, UK. Tel.: 0845 680 0971; fax: 0845 680 0972; C.H Hawkins, E.E Änggård & D.R. Harper Biocontrol Limited, BioCity, Pennyfoot Street, Nottingham, UK Tel.: 0044 207 935 4579; fax: 0044 207 935 3635
Copyright © 2009 Blackwell Publishing Ltd
Clin. Otolaryngol. 2009, 34, 349–357

Objectives: To evaluate the efficacy and safety of a therapeutic bacteriophage preparation (Biophage-PA) targeting antibiotic-resistant Pseudomonas aeruginosa in chronic otitis.

Design: Randomised, double-blind, placebo-controlled Phase I/II clinical trial approved by UK Medicines and Healthcare products Regulatory Agency (MHRA) and the Central Office for Research Ethics Committees (COREC) ethical review process.

: A single specialist university hospital.

Participants: 24 patients with chronic otitis with a duration of several years (2–58). Each patient had, at the time of entry to the trial, an ear infection because of an antibiotic-resistant P. aeruginosa strain sensitive to one or more of the six phages present in Biophage-PA. Participants were randomised in two groups of 12 treated with either a single dose of Biophage-PA or placebo and followed up at 7, 21 and 42 days after treatment by the same otologist. Ears were thoroughly cleaned on each occasion and clinical and microbiological indicators measured.

Main outcome measures: Physician assessed erythema/inflammation, ulceration/granulation/polyps, discharge quantity, discharge type and odour using a Visual Analogue Scale (VAS). Patients reported discomfort, itchiness, wetness and smell also using a VAS. Bacterial levels of P. aeruginosa and phage counts from swabs were measured initially and at follow-up. At each visit patients were asked about side effects using a structured form. Digital otoscopic images were obtained on days 0 and 42 for illustrative purposes only.

Results: Relative to day 0, pooled patient- and physician-reported clinical indicators improved for the phage treated group relative to the placebo group. Variation from baseline levels was statistically significant for combined data from all clinic days only for the phage treated group. Variation from baseline levels was statistically significant for the majority of the patient assessed clinical indicators only for the phage treated group. P. aeruginosa counts were significantly lower only in the phage treated group. No treatment related adverse event was reported.

Conclusion: The first controlled clinical trial of a therapeutic bacteriophage preparation showed efficacy and safety in chronic otitis because of chemo-resistant P. aeruginosa.

I’m Superhuman


  • Last Article of Interest Read:
    β-Alanine supplementation augments muscle carnosine content and attenuates fatigue during repeated isokinetic contraction bouts in trained sprinters

    β-Alanine supplementation aug-
    ments muscle carnosine content and attenuates fatigue during
    repeated isokinetic contraction bouts in trained sprinters. J Appl
    Physiol 103: 1736–1743, 2007. First published August 9, 2007;
    doi:10.1152/japplphysiol.00397.2007.—Carnosine (␤-alanyl- L –
    histidine) is present in high concentrations in human skeletal muscle.
    The ingestion of ␤-alanine, the rate-limiting precursor of carnosine,
    has been shown to elevate the muscle carnosine content. We aimed to
    investigate, using proton magnetic resonance spectroscopy (proton
    MRS), whether oral supplementation with ␤-alanine during 4 wk
    would elevate the calf muscle carnosine content and affect exercise
    performance in 400-m sprint-trained competitive athletes.

    J Appl Physiol 103: 1736-1743, 2007.