Such a Bro

When someone is being such a bro.

Jan 3
Alli figuring it all out; (alli does not like the photo enough to provide a caption)

Alli figuring it all out; (alli does not like the photo enough to provide a caption)


Mar 1

Dec 6

Someone already has a tumblr dedicated to amazing amazon.com reviews, but whatever.  See bolded text below.

1.0 out of 5 stars

 Beware of this scam, August 29, 2011
This review is from: John Bell and Bell’s Theorem (Kindle Edition)

The book is titled “John Bell and Bell’s theorem”, but only the last two pages of this book talk about it. And the last two pages do not give any insight into Bell’s theorem, they just mention that Bell’s theorem deals with non-locality and it’s a very important theorem. The entire book is a haphazard collection of “class notes” that have been published without any organization. The author did not bother to divide the book into chapters and sections for easy navigation. The first 98 % percent of the book appears to be a definition/discussion of science in general. However, it is the most disorganized discussion that I have ever read. The discussion just jumps from one topic to another. Organization is not the only problem, the content and language of the discussion/notes is also pathetic. For example…[ mathematics is one of the sciences that deals with numbers. The first ten numbers are 0 1 2 3 4 5 6 7 8 9… there are other numbers also. You can do different operations on numbers like add, subtract, multiply divide, and others ] Something like this can only be written by a kindergarten pupil or someone who is psychologically challenged. The entire book is filled with nonsense like this.


Nov 24
sickpapes:

Berger, T.W., Hampson, R.E., Song, D., Goonawardena, A., Marmarelis, V.Z. and Deadwyler,  S.A. “A cortical neural prosthesis for restoring and enhancing memory.” J. Neural Eng., Vol. 8, 2011.
When I was a kid I watched this TV show called “DinoRiders.” The premise was pretty simple: a fleet of human spaceships was involved in a battle with a fleet of alien spaceships, something happened and they all traveled back in time and crashed on earth. They’re back in the time of dinosaurs; the humans become friends with the dinosaurs, the aliens build these sweet devices that control dinosaur minds, both sides load up the dinosaurs with tons of lasers and missiles and shit, and the aliens and humans continue warring, riding dinosaurs instead of spaceships.
We now live in a world one step closer to that of the DinoRiders. A group from Wake  Forest and USC have been dropping pape after pape about a “cortical neural prosthesis” for rats that greatly improves their performance at a memory task.  The task was a “delayed non-match to sample” memory protocol. The rat was presented with a lever on either the left or the right (the sample target); after it pressed the lever, the lever retracted, and after a delay (10-60 s), levers appeared on both the left and the right, and if the rat pressed the lever on the opposite side from where the sample appeared (a non-match), it was rewarded. 
They implanted 8-channel electrodes that could both record and stimulate in hippocampal areas CA1 and CA3 bilaterally for a total of 32 electrodes. Backed up by a lot of previous work and their own findings, they determined that after the initial sample phase of the task, rhinal cortex feeds sensory input about which lever the rat saw through the dentate gyrus into CA3. The population of neurons in CA1 fires an output pattern in response that in some high-level manner encodes the behavioral response. Blah blah blah, that is obviously a cartoonishly simple explanation of what’s going on and doesn’t really mean anything. The researchers modeled the CA3-CA1 network as a black box where the ensemble response of recorded neurons from CA3 was mapped to the ensemble response in CA1. The model used a recurrent network of CA3-CA1 units described by a Taylor series with a long memory to capture nonlinear responses and incorporated not only covariance but also triplet co-occurrence of input neuron firing patterns.
During the initial behavioral trials, the rats first performed the nonmatch-to-sample task a number of times, and CA3 and CA1 firing patterns were recorded using the prosthesis (without stimulation). The input-output relationship between the firing patterns of sampled neurons in CA3 and CA1 was solved for using the model. They found rather distinct firing patterns in CA3 for successful and unsuccessful trials very shortly after the sample presentation. During the test trials, this fact allowed them to predict if the rat had encoded the input properly or not and whether it was going to make a successful or unsuccessful choice. On trials when the rat observed the sample and the firing pattern at CA3 indicated the rat was going to be wrong, the researchers were able to override this by stimulating a firing pattern for the correct response on CA1, which caused the rat to perform significantly better than control (this is the CL [closed-loop] strong code in the figure).
The fact that they could control the behavioral response with 32 electrodes and an (admittedly absurdly complex) computational model is in one sense unbelievable but in another completely expected. Certainly this work is so successful because the discrete behavioral task is so easy. This paper represents a remarkable confluence of advances at widely varying levels of analysis, but unfortunately it is still a long way from a system that not only allows aliens to verbally instruct a severely primitive dinosaur brain to perform complex behavioral responses in high-stress futuristic battle scenarios, but to do so with a system that operates transcranially using presumably some sort of magnetic manipulation of firing patterns on a limited volume of neural tissue. It’s a step in the right direction, though, and with recent advances in time travel, I expect to be riding in a troop carrier mounted on a Diplodocus longus flank in the next ten years.

sickpapes:

Berger, T.W., Hampson, R.E., Song, D., Goonawardena, A., Marmarelis, V.Z. and Deadwyler, S.A. “A cortical neural prosthesis for restoring and enhancing memory.” J. Neural Eng., Vol. 8, 2011.

When I was a kid I watched this TV show called “DinoRiders.” The premise was pretty simple: a fleet of human spaceships was involved in a battle with a fleet of alien spaceships, something happened and they all traveled back in time and crashed on earth. They’re back in the time of dinosaurs; the humans become friends with the dinosaurs, the aliens build these sweet devices that control dinosaur minds, both sides load up the dinosaurs with tons of lasers and missiles and shit, and the aliens and humans continue warring, riding dinosaurs instead of spaceships.

We now live in a world one step closer to that of the DinoRiders. A group from Wake Forest and USC have been dropping pape after pape about a “cortical neural prosthesis” for rats that greatly improves their performance at a memory task.  The task was a “delayed non-match to sample” memory protocol. The rat was presented with a lever on either the left or the right (the sample target); after it pressed the lever, the lever retracted, and after a delay (10-60 s), levers appeared on both the left and the right, and if the rat pressed the lever on the opposite side from where the sample appeared (a non-match), it was rewarded. 

They implanted 8-channel electrodes that could both record and stimulate in hippocampal areas CA1 and CA3 bilaterally for a total of 32 electrodes. Backed up by a lot of previous work and their own findings, they determined that after the initial sample phase of the task, rhinal cortex feeds sensory input about which lever the rat saw through the dentate gyrus into CA3. The population of neurons in CA1 fires an output pattern in response that in some high-level manner encodes the behavioral response. Blah blah blah, that is obviously a cartoonishly simple explanation of what’s going on and doesn’t really mean anything. The researchers modeled the CA3-CA1 network as a black box where the ensemble response of recorded neurons from CA3 was mapped to the ensemble response in CA1. The model used a recurrent network of CA3-CA1 units described by a Taylor series with a long memory to capture nonlinear responses and incorporated not only covariance but also triplet co-occurrence of input neuron firing patterns.

During the initial behavioral trials, the rats first performed the nonmatch-to-sample task a number of times, and CA3 and CA1 firing patterns were recorded using the prosthesis (without stimulation). The input-output relationship between the firing patterns of sampled neurons in CA3 and CA1 was solved for using the model. They found rather distinct firing patterns in CA3 for successful and unsuccessful trials very shortly after the sample presentation. During the test trials, this fact allowed them to predict if the rat had encoded the input properly or not and whether it was going to make a successful or unsuccessful choice. On trials when the rat observed the sample and the firing pattern at CA3 indicated the rat was going to be wrong, the researchers were able to override this by stimulating a firing pattern for the correct response on CA1, which caused the rat to perform significantly better than control (this is the CL [closed-loop] strong code in the figure).

The fact that they could control the behavioral response with 32 electrodes and an (admittedly absurdly complex) computational model is in one sense unbelievable but in another completely expected. Certainly this work is so successful because the discrete behavioral task is so easy. This paper represents a remarkable confluence of advances at widely varying levels of analysis, but unfortunately it is still a long way from a system that not only allows aliens to verbally instruct a severely primitive dinosaur brain to perform complex behavioral responses in high-stress futuristic battle scenarios, but to do so with a system that operates transcranially using presumably some sort of magnetic manipulation of firing patterns on a limited volume of neural tissue. It’s a step in the right direction, though, and with recent advances in time travel, I expect to be riding in a troop carrier mounted on a Diplodocus longus flank in the next ten years.


Sep 28
my new joint
sickpapes:

Stevens, J.K. and Emerson, R.C. and Gerstein, G.L. and Kallos, T. and Neufeld, G.R. and Nichols, C.W. and Rosenquist, A.C., “Paralysis of the Awake Human: Visual Perceptions”, Vision Research, 1976. (pdf)
A while ago, Sick Papes expressed enthusiasm for the storied scientific tradition of pushing on your eyeball until you see crazy shit.  Eye-pushers in ancient Greece convinced everyone that so-called deformation phosphenes were evidence that the eye itself was generating light, until Kepler, Newton and Descartes (among others) finally realized that mechanical deformation activated the same sort of tissue in the eye that light triggers.
Helmholtz, another eminence grise among eye-pushing natural philosophers, also noticed that with one eye closed, a few rapid pokes with one’s finger (not strong enough to elicit phosphenes) to the outer part of the open eye generate an odd perception that the world is jumping about.  Obviously this does not occur when one moves one’s eyes normally with voluntary extraocular muscles.  Helmholtz put forth the theory of efference copy: the motor control signals sent to the eye muscles are used to compensate for the change in the perceived visual world that they cause.  The world doesn’t look like it’s jumping around during eye movements.  The observer’s perception of position will not be affected by the change in the visual world as a result of eye movements.
A bunch of bros at UPenn replicated previous work and performed several new experiments taking Helmholtz’s idea in the other direction.  What happens if you try to move your eyes when they cannot move?  Before they began the experiments described in this pape,
a) they told at-the-time graduate student John K. Stevens that he had to subject himself to total paralysis with sundry neurotoxins in order to keep his funding, or
b) they were lucky they had Stevens, who eagerly agreed to an NIH-sponsored exercise in drug-induced total paralysis at a cozy hospital research laboratory-cum-opium den with a bunch of chill enabler-type yet sober and competent doctors on hand should anything happen to go wrong.  
I hope it was the latter.  To be fair, two of the other authors also underwent partial paralysis along with Stevens.  In the partial paralysis condition, they were given a number of doses of curare, a nerve toxin used by hunters in South America that is an ACh blocker and therefore muscle relaxant.  For the most part they could still walk around and talk, even as their eye movements were affected. They reported “low doses of curare were not at all unpleasant.” 
In the full paralysis condition, shit got real.  Curare requires some time to take effect, so with the periodic injection procedure they used, when aiming for full paralysis there was a slight risk of something going wrong (i.e., death).  Instead, succinylcholine, another ACh blocker, but one that works quickly and is a bit safer, was used.  Unfortunately, when that shit hits it hits you hard in the form of powerful muscle spasms.  Apologies to the physiologists if I butcher this, but succinylcholine is a depolarizing ACh blocker, which I presume causes the spasms, while curare is non-depolarizing, so Stevens was first given curare to ease him into the real shit and prevent spasms. Total paralysis required him to be on a respirator, and, because he couldn’t speak, he put a tourniquet on his right arm so that it wouldn’t be paralyzed and he’d have a way to communicate with his co-experimenters.  Oh, and they made him do the whole full paralysis thing on three separate occasions, basically because they thought he was too weak and not trying hard enough to move his eyes when he was actually just paralyzed.
Anyway, they got some intriguing results.  They used a strange form of eye tracking with a mirrored contact lens (see artist’s conception; note moustache).  In the partial paralysis condition, all three subjects reported seeing the world “jump” after an attempted saccade.  In the full paralysis condition, interestingly, this was not experienced by Stevens.  They reasoned that the jumping was only occurring after successful saccades.  Immediately preceding, during and following a saccade, the data in the optic nerve is not available consciously (which is why it is impossible to see one’s eyes moving in a mirror; and it’s actually only the low spatial frequency data that is suppressed).  The “jumping”, they reasoned, was the experiential component of what happens when saccadic suppression is inactivated.  
They claimed to have resolved a debate as to whether suppression is triggered by an efference copy from the extraocular motor control signal or by fast temporal motion of images on the retina in favor of the latter hypothesis.  As curare doses increased, saccadic movement slowed to the point where the image motion across the retina was not sufficient to trigger suppression, despite the continued activation of extraocular muscles.  If suppression were triggered by the efference copy, the “jumping” of the visual scene would not have been observed. Unfortunately, they did not take into account the fact that saccadic suppression is evident even before the saccade is made and blurring of the image would not occur until after the saccade has begun.  Later experiments by others conclusively demonstrated that suppression is indeed caused by the efference copy of the motor signal to move the eyes.
In the full paralysis condition, Stevens reported a slow “displacement” of the world occurred after he attempted to saccade but could not.  Since he could not move his eyes, there was no shift in his visual world.  “Pure displacement is not normally experienced and thus very hard to describe.  It is not necessarily visual in nature, but simply the feeling that if you wanted to touch a given object, you would have to reach to the right, left, up or down etc.” So… something of an ineffable quale.  By comparing this experience to the partial paralysis condition, it is evident that this displacement sensation was a result of the efference copy of the extraocular muscles unaccompanied by the actual shift in the visual field. 
A few years later, Stevens was the first author on a paper published in Science using the same paradigm in which they looked at perception under paralysis in darkness.  It’s been reported that Stevens recently left his post as a full professor at the University of Toronto to start a company that specializes in boutique altered-state experiences, and as an optimistic future customer I wish him the best of luck.

my new joint

sickpapes:

Stevens, J.K. and Emerson, R.C. and Gerstein, G.L. and Kallos, T. and Neufeld, G.R. and Nichols, C.W. and Rosenquist, A.C., “Paralysis of the Awake Human: Visual Perceptions”, Vision Research, 1976. (pdf)

A while ago, Sick Papes expressed enthusiasm for the storied scientific tradition of pushing on your eyeball until you see crazy shit.  Eye-pushers in ancient Greece convinced everyone that so-called deformation phosphenes were evidence that the eye itself was generating light, until Kepler, Newton and Descartes (among others) finally realized that mechanical deformation activated the same sort of tissue in the eye that light triggers.

Helmholtz, another eminence grise among eye-pushing natural philosophers, also noticed that with one eye closed, a few rapid pokes with one’s finger (not strong enough to elicit phosphenes) to the outer part of the open eye generate an odd perception that the world is jumping about.  Obviously this does not occur when one moves one’s eyes normally with voluntary extraocular muscles.  Helmholtz put forth the theory of efference copy: the motor control signals sent to the eye muscles are used to compensate for the change in the perceived visual world that they cause.  The world doesn’t look like it’s jumping around during eye movements.  The observer’s perception of position will not be affected by the change in the visual world as a result of eye movements.

A bunch of bros at UPenn replicated previous work and performed several new experiments taking Helmholtz’s idea in the other direction.  What happens if you try to move your eyes when they cannot move?  Before they began the experiments described in this pape,

a) they told at-the-time graduate student John K. Stevens that he had to subject himself to total paralysis with sundry neurotoxins in order to keep his funding, or

b) they were lucky they had Stevens, who eagerly agreed to an NIH-sponsored exercise in drug-induced total paralysis at a cozy hospital research laboratory-cum-opium den with a bunch of chill enabler-type yet sober and competent doctors on hand should anything happen to go wrong. 

I hope it was the latter.  To be fair, two of the other authors also underwent partial paralysis along with Stevens.  In the partial paralysis condition, they were given a number of doses of curare, a nerve toxin used by hunters in South America that is an ACh blocker and therefore muscle relaxant.  For the most part they could still walk around and talk, even as their eye movements were affected. They reported “low doses of curare were not at all unpleasant.” 

In the full paralysis condition, shit got real.  Curare requires some time to take effect, so with the periodic injection procedure they used, when aiming for full paralysis there was a slight risk of something going wrong (i.e., death).  Instead, succinylcholine, another ACh blocker, but one that works quickly and is a bit safer, was used.  Unfortunately, when that shit hits it hits you hard in the form of powerful muscle spasms.  Apologies to the physiologists if I butcher this, but succinylcholine is a depolarizing ACh blocker, which I presume causes the spasms, while curare is non-depolarizing, so Stevens was first given curare to ease him into the real shit and prevent spasms. Total paralysis required him to be on a respirator, and, because he couldn’t speak, he put a tourniquet on his right arm so that it wouldn’t be paralyzed and he’d have a way to communicate with his co-experimenters.  Oh, and they made him do the whole full paralysis thing on three separate occasions, basically because they thought he was too weak and not trying hard enough to move his eyes when he was actually just paralyzed.

Anyway, they got some intriguing results.  They used a strange form of eye tracking with a mirrored contact lens (see artist’s conception; note moustache).  In the partial paralysis condition, all three subjects reported seeing the world “jump” after an attempted saccade.  In the full paralysis condition, interestingly, this was not experienced by Stevens.  They reasoned that the jumping was only occurring after successful saccades.  Immediately preceding, during and following a saccade, the data in the optic nerve is not available consciously (which is why it is impossible to see one’s eyes moving in a mirror; and it’s actually only the low spatial frequency data that is suppressed).  The “jumping”, they reasoned, was the experiential component of what happens when saccadic suppression is inactivated. 

They claimed to have resolved a debate as to whether suppression is triggered by an efference copy from the extraocular motor control signal or by fast temporal motion of images on the retina in favor of the latter hypothesis.  As curare doses increased, saccadic movement slowed to the point where the image motion across the retina was not sufficient to trigger suppression, despite the continued activation of extraocular muscles.  If suppression were triggered by the efference copy, the “jumping” of the visual scene would not have been observed. Unfortunately, they did not take into account the fact that saccadic suppression is evident even before the saccade is made and blurring of the image would not occur until after the saccade has begun.  Later experiments by others conclusively demonstrated that suppression is indeed caused by the efference copy of the motor signal to move the eyes.

In the full paralysis condition, Stevens reported a slow “displacement” of the world occurred after he attempted to saccade but could not.  Since he could not move his eyes, there was no shift in his visual world.  “Pure displacement is not normally experienced and thus very hard to describe.  It is not necessarily visual in nature, but simply the feeling that if you wanted to touch a given object, you would have to reach to the right, left, up or down etc.” So… something of an ineffable quale.  By comparing this experience to the partial paralysis condition, it is evident that this displacement sensation was a result of the efference copy of the extraocular muscles unaccompanied by the actual shift in the visual field. 

A few years later, Stevens was the first author on a paper published in Science using the same paradigm in which they looked at perception under paralysis in darkness.  It’s been reported that Stevens recently left his post as a full professor at the University of Toronto to start a company that specializes in boutique altered-state experiences, and as an optimistic future customer I wish him the best of luck.


Sep 27
Ape index in RGB

Ape index in RGB


joemande:

There’s a poll currently taking place [voting is now over] on Randy Moss’ website and I think it might be my favorite poll ever conducted.
67% think it’s 80%,  17% think it’s 50%. Only 5% think it’s 25%, while a shocking 11% think it’s 10%.

joemande:

There’s a poll currently taking place [voting is now over] on Randy Moss’ website and I think it might be my favorite poll ever conducted.

67% think it’s 80%,  17% think it’s 50%. Only 5% think it’s 25%, while a shocking 11% think it’s 10%.


Jul 16
Drinking narragansett and reading about them in my sublessor’s notebook

Drinking narragansett and reading about them in my sublessor’s notebook


May 26
Can you figure out the appropriate orientation?

Can you figure out the appropriate orientation?


May 19
This guy beat me in pool right bedfore this was taken.

This guy beat me in pool right bedfore this was taken.


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