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OfflineKingKnowledge
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KingKnowledge's Weekly Random Lectures * 1
    #21291102 - 02/17/15 10:06 PM (9 years, 1 month ago)

Hello everyone!

Partly out of boredom and partly out of my desire to share interesting intellectual phenomena with my fellow shroomerites, I will be updating this thread once a week or so with a quick lesson in an area that I believe you may find stimulating! I'll start with some neuroscience, but the topics will be very diverse: I promise!

:pipesmoke::cheers:

First Topic: Tip of the Tongue!

I'm sure you are all familiar with this annoying phenomenon - when you are so close to thinking of the right word to say, but you just can't remember it for the life of you. Well, don't be disheartened - you're not stupid or forgetful! The tip of the tongue phenomenon is a very prevalent occurrence, and a lot of research in the neuroscience field has gone into explaining why it happens. The most plausible, evidence-based hypothesis for the tip of the tongue hypothesis is quite easy to understand.

:cookiemonster:  :psychsplit:  :pipesmoke:

First, it's crucial to understand that some neurons have a function called lateral inhibition. Basically, when one neuron is fired, it shuts off, or "blocks", the neurons around it. This function, evolutionarily, is meant to stop excited neurons from passing on action potentials to neighboring neurons that aren't necessarily being targeted, but in fact, it has several other side effects including that feeling of having something at the tip of your tongue!



When the tip of the tongue phenomenon happens, you actually are activating a neuron associated with a word VERY SIMILAR to the word you are trying to think of, and this neuron consequently laterally inhibits the correct word! So when you are really struggling to think of the right word, it isn't your fault. Your neurons are physically blocking the right neuron from being activated! The best way to solve this issue is, therefore, to stop thinking about the word for a while so that the neurons of the similar words lose their activation, giving you a second chance to activate the right word in a few minutes!

Edited by KingKnowledge (03/18/15 09:03 PM)

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OfflineKingKnowledge
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Re: KingKnowledge's Weekly Random Lectures [Re: KingKnowledge] * 1
    #21344456 - 02/28/15 04:26 PM (9 years, 1 month ago)

Second Topic: Pythagorean Triples!

Warning: This topic is meant to appeal to the math nerds!

I assume all of you know the Pythagorean Theorem; you know, that thing you learned in middle school geometry that says the sum of the squares of the two legs of a right triangle equals the square of the hypotenuse. Well, it's actually a pretty cool theorem with some interesting history.

First of all, this theorem dates way before Pythagoras. There are quite a lot of Babylonian artifacts that contain big numbers that satisfy the relationship between a, b, and c -- clearly they had a reliable method to produce them. Later on, the Egyptians even utilized this theorem by taking a rope, marking 12 even segments, and holding it taught at three points to form a triangle with the common Pythagorean Triple (sides equal to 3, 4, and 5). Quite the handy architect tool.



The Pythagorean Theorem is definitely a useful relationship to know, but like any equation, it can be manipulated to show several more implications. Let's go through a baby proof to show one example.

First, let's look at a few examples of Triples that obey the Pythagorean Theorem.

(3, 4, 5)        (5, 12, 13)        (7, 24, 25)

Notice anything? Well, its clear that in these cases, c = b+1. This characteristic is common to Pythagorean Triples, so let's use it to find some insight into how to quickly find triples.

So if c=b+1, we can substitute into the Pythagorean Theorem to give:
a2 + b2 = (b+1)2.

The right side of the equation can be expanded to give us the following:
a2 + b2 = b2 + 2b + 1

Subtracting b2 from each side of the equation, we are left with:
a2 = 2b + 1

Therefore:
b = (a2 - 1)/2

We have just used an observation of a common trait of Pythagorean Triples to give us a formula to generate as many Primitive Pythagorean Triples as we want! When I say primitive, I mean that the triple has no common factors, and thus cannot be reduced down any further (think 3,4,5 compared to 6,8,10):

a = k
b = (k2 -1) / 2
c = ((k2 -1) / 2) + 1


Just pick a k, and this formula will give you two other numbers (b, c) that fulfill the Pythagorean Theorem. It's a pretty nifty equation to keep in mind if you're ever doing trigonometry, building things, or just messing around with math.

Edited by KingKnowledge (03/01/15 11:31 AM)

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Re: KingKnowledge's Weekly Random Lectures [Re: KingKnowledge]
    #21347002 - 03/01/15 07:09 AM (9 years, 30 days ago)

cool thread. In the second line that appears below

Quote:

KingKnowledge said:


So if c=b+1, we can substitute into the Pythagorean Theorem to give:
a2 + b2 = (b+1)2.

The right side of the equation can be expanded to give us the following:
a2 + b2 = (b+1)2 + 2b + 1

Subtracting b2 from each side of the equation, we are left with:
a2 = 2b + 1






I assume you meant..

the right side of the equation can be expanded to give us the following:
a2 + b2 = b2 + 2b + 1

i.e. b rather than (b+1) squared


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OfflineKingKnowledge
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Re: KingKnowledge's Weekly Random Lectures [Re: leschampignons]
    #21347830 - 03/01/15 11:32 AM (9 years, 30 days ago)

Thank you leschampignons for the correction! You are absolutely correct seeing as (b+1)2 "foils" out to b2 + 2b + 1.

I went ahead and edited the post to fix my mistake.

Edited by KingKnowledge (03/08/15 02:55 PM)

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Re: KingKnowledge's Weekly Random Lectures [Re: KingKnowledge]
    #21377807 - 03/08/15 11:25 AM (9 years, 23 days ago)

Third Topic: Dopaminergic Pathways!

Well, I assume most people on the shroomery are at least somewhat interested in neuroscience, seeing as both psychedelic and non-psychedelic drugs have profound effects on the chemistry and wirings of our brain. One of the major neurotransmitters in our brain is dopamine (DA). Dopamine is largely responsible for our sense of reward. Specifically, new studies show that DA is more directly related to the anticipation of a desired reward. This debate is often referred to as the "seeking" versus "liking" problem, where DA plays a larger role in seeking a reward rather than actually enjoying it.

In the brain, there are several major dopaminergic pathways that are important for neuroscience lovers to be familiar with. First is the mesolimbic pathway, which transmits dopamine from the Ventral Tegmental Area (VTA) of the midbrain, to the nucleus accumbens in the ventral striatum. The nucleus accumbens is a well-known portion of what is commonly referred to as the limbic system of the brain, largely responsible for reward, pleasure, emotion, and motivation, among other things. It is also important to note that this mesolimbic pathways is linked to psychosis! Increased DA transmission elicits psychosis in healthy subjects and exacerbates positive symptoms in schizophrenic patients.

A second major dopaminergic pathway is called the mesocortical pathway, leading dopaminergic transmission from the VTA to the frontal cortex! This pathway is involved in cognitive functioning, as well as the negative symptoms of schizophrenia. When I say negative symptoms, I refer to the lack of normal functioning (such as blunted affect, asociality, and emotional withdrawal).

Sidenote on Schizophrenia
One major theory of schizophrenia explains that the disorder is characterized by hypofrontality and hyperactive mesolimbic transmission. In other words, there is too little dopamine in the mesocortical pathway (the frontal lobe), and too much dopamine in the striatum and nucleus accumbens (in the limbic system).

The final dopaminergic pathway to consider, especially in cases of schizophrenia, is the nigrostriatal pathway. This pathway transmits dopamine from the substantia nigra to the striatum, and is largely responsible for motor control. When you hear about the inability to maintain motor control in Parkinson's Disease or with Extra-Pyramidal Symptoms of taking anti-psychotic drugs (EPS), this is due to irregularities to the nigrostriatal pathway.

:philososloth:

Obviously this is a very concise and condensed summary of the dopaminergic pathways, but these pathways play a crucial role in schizophrenia, as well as drug addiction, anhedonia (the inability to feel pleasure), loss of motivation, and many other psychiatric prognoses!

Stay tuned for a new lesson next week!

Edited by KingKnowledge (03/18/15 09:08 PM)

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OfflineKingKnowledge
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Re: KingKnowledge's Weekly Random Lectures [Re: KingKnowledge]
    #21426382 - 03/18/15 11:40 AM (9 years, 13 days ago)

Fourth Topic: Addicted to Cigarettes: Not What You'd Think!


When you are dying for a cigarette, it might not be nicotine that your brain is craving! What if you were just being tempted by cues in the environment that remind you of cigarettes? Well, research over the past few years lends substantial evidence to this possibility.

Quick Neuroscience Lesson

The receptors that nicotine attaches to in the brain are called nicotinic acetylcholine receptors (nAChR's). Out of the many types of acetylcholine receptors, the α4β2 nAChR is the most important for our purposes because it has the highest affinity for nicotine out of any receptor (AKA they attract it the most!).These receptors are found (not exclusively) on dopamine neurons in the Ventral Tegmental Area (which I mentioned in my first lecture as a portion of the system responsible for reward/anticipation), and they are activated by acetylcholine and, when you smoke, nicotine.

When you smoke only 15% of a cigarette, more than half of your α4β2 receptors will be fully occupied, giving 50% of the dopamine rush. Smoking a full cigarette causes >90% receptor occupancy. So...if its so easy to achieve a cigarette "buzz" with only a tiny bit of nicotine, why do people feel the urge to smoke packs a day?

:smokerage:

The reason is easy to see if you understand the phenomenon of desensitization, or when a receptor that is constantly being flooded with neurotransmitters becomes less sensitive to the same amount of neurotransmitter release. This process is accompanied by a decrease in the number of receptors (deregulation) as the body reacts to excessive neurotransmitter transmission. Since these high-affinity α4β2 receptors are being stimulated so often when you smoke, they become so desensitized that they are barely activated anymore by nicotine, which in turn leads to very little dopamine release in the VTA.

However, this desensitization affects other neurotransmitters than dopamine. For example, acetylcholine also projects to α4β2 receptors on GABA neurons - an inhibitory neuron. When α4β2 desensitization of these GABA neurons causes less GABA activation and therefore LESS TONIC INHIBITION of dopamine, this means that the dopamine neuron can now be easily activated by any additional excitatory input, which just so happens to be glutamate!

I'm almost done, I promise

Glutamate input from the prefrontal cortex and the amygdala project onto the same VTA dopamine neurons, and provide information about nicotine-associated cues! That means that whenever you are reminded of any cue about smoking (from your environment, setting, friends, etc), glutamate projects onto these VTA neurons and has a larger affect than normal due to less GABA inhibition. In conclusion, you get a bigger rush of dopamine than usual from environmental cues related to smoking cigarettes if your α4β2 receptors are desensitized, which reminds you to have a smoke. (Well, it makes you crave nicotine, but we can get into addiction in another topic).

:smoker:  :smoker:  :smoker:  :pipesmoke:  :pipesmoke:  :pipesmoke:

I know this topic was kinda complicated, but I thought you guys would be interested in seeing how nicotine addiction starts to unavoidably creep in! Until next time...and please ask questions/comment! Suggestions welcome.

Edited by KingKnowledge (03/18/15 06:23 PM)

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Re: KingKnowledge's Weekly Random Lectures [Re: KingKnowledge]
    #21431848 - 03/19/15 03:47 PM (9 years, 12 days ago)

lovin this thread. Thanks for doing this.  :thumbup:


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Re: KingKnowledge's Weekly Random Lectures [Re: leschampignons]
    #21436216 - 03/20/15 03:34 PM (9 years, 11 days ago)

Thank you for following the thread! Hopefully I can get a few other people interested too...:lol:

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Re: KingKnowledge's Weekly Random Lectures [Re: KingKnowledge]
    #21440985 - 03/21/15 08:32 PM (9 years, 9 days ago)

Ah so this explains why it is easier for some to quit than others. Once you are used to smoking while doing things like driving or talking on the phone it is these environmental factors to trigger your 'addiction'!


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Re: KingKnowledge's Weekly Random Lectures [Re: AGUARES]
    #21444934 - 03/22/15 09:44 PM (9 years, 8 days ago)

Quote:

AGUARES said:
Ah so this explains why it is easier for some to quit than others. Once you are used to smoking while doing things like driving or talking on the phone it is these environmental factors to trigger your 'addiction'!




Well that's certainly one of the factors, but not the only thing that accounts for individual variability in quitting a drug/being addicted.

A lot of addiction boils down to genetics. Some people are just wired differently, in terms of their dopaminergic functioning and the salience of different stimuli.

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Re: KingKnowledge's Weekly Random Lectures [Re: KingKnowledge]
    #22278785 - 09/23/15 01:10 PM (8 years, 6 months ago)

I miss these.  :frown:


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Re: KingKnowledge's Weekly Random Lectures [Re: leschampignons]
    #22282579 - 09/24/15 08:29 AM (8 years, 6 months ago)

Quote:

leschampignons said:
I miss these.  :frown:




Took a break from the shroomery for a while but stay tuned :wink:

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Re: KingKnowledge's Weekly Random Lectures [Re: KingKnowledge]
    #22282653 - 09/24/15 08:51 AM (8 years, 6 months ago)

Fifth Topic: Half Asleep and Half Awake

Ever wish you could multi-task during sleep? Well, unfortunately us humans don't have that capability. When we sleep, we are knocked out completely. Yes we have dreams and some of us even sleep walk, but that is certainly not the same as keeping one half of your brain awake during sleep. Believe it or not, several species on this planet have evolved to perform this act that has been labeled Unihemispheric Slow Wave Sleep.

:sleep:  :sleep:  :sleep:

During Unihemispheric Slow Wave Sleep, an animal sleeps with one half of the brain while the other half remains conscious and alert. While one eye goes through a period of non-rapid eye movement, the other eye remains open and receptive to exogenous stimuli. Pretty cool, eh?

:pipesmoke: :pipesmoke:

Well, the reason humans aren't able to perform this extraordinary feat is because we have no evolutionary incentive to do so. The same cannot be said for the Amazon River Dolphin, the Beluga Whale, the Porpoise, the Southern sea lion, the Japanese quail, the common blackbird, and a handful of other species who constantly face the risk of predation. If these animals were to simply fall into a multi-hour period of deep, unaware, unprotected sleep, they would surely be eaten by larger and more dangerous predators. In a response to this constant threat, these animals have evolved to remain alert around the clock, keeping one eye open at all times. In fact, the half of the brain associated with this eye is completely aware of its surroundings. In experiments where ducks were arranged in a line during sleep, the ducks with the highest risk of predation on the outsides of the group awoke from sleep when they were presented an object that looked like it was getting bigger (to imitate a predator's attack). This sleep phenomenon is hard-wired into their brains through centuries of survival.



This adaptation doesn't only serve to mitigate the risk of predation. In fact, several species of birds will fall into a state of unihemispheric slow wave sleep during long migrations. Did you catch that? Birds will literally put half of their brains to sleep while they are flying thousands of miles. How's that sound for autopilot?

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Re: KingKnowledge's Weekly Random Lectures [Re: KingKnowledge]
    #22282894 - 09/24/15 09:42 AM (8 years, 6 months ago)

:popcorn: :takingnotes:
How intriguing!


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Re: KingKnowledge's Weekly Random Lectures [Re: KingKnowledge]
    #22282910 - 09/24/15 09:45 AM (8 years, 6 months ago)

Kudos on this thread. Keep it coming. (:

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Re: KingKnowledge's Weekly Random Lectures [Re: Mental Taco]
    #22284977 - 09/24/15 05:23 PM (8 years, 6 months ago)

Quote:

Mental Taco said:
:popcorn: :takingnotes:
How intriguing!



:whathesaid:

:awethumb:


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Re: KingKnowledge's Weekly Random Lectures [Re: leschampignons]
    #22305351 - 09/28/15 09:30 PM (8 years, 5 months ago)

This thread...is....awesome.


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Re: KingKnowledge's Weekly Random Lectures [Re: goldcaphunter]
    #22746883 - 01/07/16 02:37 AM (8 years, 2 months ago)

:takingnotes:

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Re: KingKnowledge's Weekly Random Lectures [Re: shellzenone]
    #22750331 - 01/07/16 09:32 PM (8 years, 2 months ago)

Next post should be coming in the upcoming week...sorry! Busy times.

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Re: KingKnowledge's Weekly Random Lectures [Re: KingKnowledge]
    #22750836 - 01/08/16 12:11 AM (8 years, 2 months ago)

This is kinda like vsauce on youtube lol!

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Re: KingKnowledge's Weekly Random Lectures [Re: shellzenone]
    #22781474 - 01/15/16 08:38 AM (8 years, 2 months ago)

Awesome!  Awaiting more!


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Re: KingKnowledge's Weekly Random Lectures [Re: dhype773]
    #22817088 - 01/23/16 09:53 PM (8 years, 2 months ago)

Sixth Topic: Neuroplasticity and Echo-Location

Neuroscience is arguably the last frontier of modern-day science. Only as recently as 1991 did we first discover tools (the fMRI) to better understand the workings of our brains. Although hundreds of thousands of scientific articles have been published over the past two decades in an attempt to understand how our brains react to everyday information, there are still many questions left to be answered. How did we, a seemingly random species on this diverse planet, develop consciousness? How have we evolved to remember, to feel emotion, to question the very existence of our being?

Some of these questions may never be answered. However, one of the most fascinating revelations that we have arrived at over the past few years is the astounding fact that our brains may not be as rigid as we think. In fact, the very structure and organization of our brains have been found to be malleable. Our brains are, for lack of a better term, plastic.



Neuroplasticity is a recently-coined term that is used to explain how our brains continue to adapt throughout our lives. Scientists used to believe that we underwent certain "critical periods" during childhood, and that after these periods were done, our brains were finished developing! Unchangeable! But today, there is an enormous body of evidence that says otherwise. Now, neuroplasticity is an enormous topic that can explain countless phenomenon, so I just picked one of the most fascinating ideas to share with you today:

Echolocation....in humans

Now, we've all heard about how bats and dolphins can use echolocation to sense their surroundings without actually seeing them. But echolocation in humans? You've got to be crazy.....or maybe you're just smart. Although we've studied human echolocation since the 1950s, we've only recently figured out a way to explain this amazing phenomenon. Here's the quick summary:



Your visual cortex is a part of your brain in the back of your head that is responsible for almost everything that you see. Although a very simplified explanation, the visual cortex takes stimuli from your retinas and maps out this information in a way that allows you to see the world around you! Now, all that is fine and dandy, but what if you are blind? What if, for some reason, the visual cortex can't receive that information from your retinas? Does that part of the brain just not do anything for blind people?



Well, thanks to neuroplasticity, those who suffer from blindness aren't as in the dark as it may seem! MRI studies over the past 5 years have shown that the visual cortex actually can take on new roles when someone turns blind! In terms of human echolocation, scientists have found that the visual cortex goes through a slow but sure transformation when someone becomes blind. Rather than simply taking up space in the brain without processing information, the visual cortex begins to receive input from other stimuli. Now, in a normal brain, the auditory cortex, or the part of the brain that processes sounds, is far away from the visual cortex. But in blind people, the visual cortex can start to process sounds instead of spatial information! Talk about a plastic brain.

Don't believe me? Well, Daniel Kish was born in 1966, and in 1967, he had both of his eyes removed due to retinal cancer. Daniel certainly can't see the way we do, but he is an avid hiker and mountain biker. How the hell can a blind person do that? Well, Kish started off making clicking sounds with his tongue. He would click everywhere he went, and eventually, he started to get a rich, vivid understanding of his surroundings. It's like he could see through sound! Kish eventually started carrying around a cane, tapping it around everywhere so that he could sense the echoes bouncing off nearby objects. If you think he's lying, Kish can even tell the difference between different materials such as wood and metal by the information returned by the echoes. When scientists put Kish in an fMRI machine, they determined that "brain structures that process visual information in sighted people process echo information in blind...experts".



Echo-location is only one of the amazing phenomena that our brains have adapted to learn. Neuroplasticity is a beautiful thing, and it allows us to face challenges in our life with the knowledge that our brains are wired to overcome, no matter how high the obstacle.

Edited by KingKnowledge (01/23/16 10:03 PM)

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Re: KingKnowledge's Weekly Random Lectures [Re: KingKnowledge]
    #23007100 - 03/14/16 07:33 PM (8 years, 15 days ago)

Aw dude,

you should do Logical Paradoxes. That would be cool.

"Suppose you walk past a barber's shop one day, and see a sign that says

"Do you shave yourself? If not, come in and I'll shave you! I shave anyone who does not shave himself, and noone else."
This seems fair enough, and fairly simple, until, a little later, the following question occurs to you - does the barber shave himself? If he does, then he mustn't, because he doesn't shave men who shave themselves, but then he doesn't, so he must, because he shaves every man who doesn't shave himself... and so on. Both possibilities lead to a contradiction."


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To do; DMT, DPT, 2C-B, Ro5-4864, alprazolam, DOM/DOB, Tramadol, MDMA, Candy Flipping, BROMO-DragonFly, 2-CB-FLY

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