#compromised mirror neurons

[mumblelard]

i think clarice produced a bud just to keep ruth company

[pyxxiestyxx]

Class-C

The shot glass sat in front of you, innocuous in appearance.  If you couldn't smell the tang of citrus, if you didn't catch the occasional sparkle suspended in it, you might think it mere water.

In front of you, your affini friend rested her head on her hand.  She practically bled smugness, the leaves around her neck slightly fluffed as if she was preening.  You rolled your eyes, mirroring her posture for the hell of it.

"So this is your bet?  Aren't Class-C's something on the 'dont mess with' list for terrans anyway?"

Her voice was a rolling purr as she answered, "Yes.  This is different.  A heavily diluted solution of a specific strain.  No lasting effects, just the intense feeling of a Class-C dose for about two hours."

The bet was simple: You had to make it through thirty minutes without confessing your love for her, or begging to be her floret.   She thought you couldn't do it.  You thought she was full of shit.  You had plenty of xenodrugs before, of course.  Class A's and E's were fun and relaxing, but ultimately you were still in control of things.

Shrugging nonchalantly, you picked up the shot and threw it back, the sweet flavor hitting your throat and tingling slightly as it went down.  You flipped the glass face down and slammed it onto the table, then looked up at her with a satisfying smirk.  "Easy."

Her smile only widened.  "We'll see." She flipped open her tablet and pressed a timer, starting a countdown clock.  She showed you it had thirty minutes remaining, then flipped it closed.  "No using the time you have left for rallying cries.  Just you, me, and the lovely chemicals your brain is about to be swimming in.  When the alarm rings, I'll administer the counteragent."

You scoffed, leaning back in my chair.  "You didn't even wait until it had begun to kick in?  Wow, you must really be confident."

"Oh, it begins nearly immediately.  Already the drug is interacting with those neurons, mixing in with seratonin and oxytocin and a few other things besides."

You looked at her, doubtful.  "Yeah?  Then how come I don't feel any different?"

"Sweetie, you've leaned halfway across the table already.  Move any further and you're likely to crush that shot glass you slammed down so viciously earlier." She gestured at your posture, causing you to hurriedly sit back into your chair with a blush.

"Shit, I...sorry.  Got carried away." You glanced down at the shot glass, biting your lip as you realized that you *had* been rather violent with it.  You carefully flipped it back upright, wiping the outside clean with your shirt.  "Um.  Sorry."

"Dear, did you just apologize to the glas-"

"NO!" Your face was properly red now.  Oh *stars*, you had!  You had just done something that embarrassing in front of your Best Friend and what if she thought you were silly now?  Would she not want to hang out with you?  You hoped not.  You really enjoyed her compa....wait....

Frowning, you shook your head roughly, slapping your cheeks a little.  It was just the drug.  You were in control.  The drugs were doing this.  But unlike the A or E, it was more...subtle.  or rather, it was potent, but you didn't even realize it until your best friend had pointed it out.  Gosh, she's so kind...

"Um, t-thank you for helping me remember I was drugged." The words felt good to say.  You wanted her to know how much you appreciated her after all.  So you could win the bet!

...

The bet?

"Wait, what happens if I lose?" You realized you had forgotten to ask that before.  Worried, you turned to look at her.

"Well, what would you like to happen, pet~al?" You blushed, realizing it was just like her to wait until you were...compromised before asking this.  Well, jokes on her!  You're still in control.

"Nothing!  I don't want anything to happen.  No new rules, no teasing, and no domestication.  Got it?"

She nodded, sagely.  "Of course.  In that case, I take that to mean that should you win, you'll get all of those wonderful things~"

You sputtered in shock.  "I- no! I don't want to... I'm...you can't be serious."

"Awww, is something wrong?" She smirked, her eyes flashing purples and golds in a way that made your heart melt.  "All you have to do now is lose, then~ Or are you so stubborn, you can't admit that you l~o~v~e me, flower?"

"I-I...you... fucking...."  You felt the indignation mix with the heady joy of her attention, of wanting to give into her, of wanting to beg.  She was trying to goad you.  She wanted you to win now.  She had entirely turned the rules on their head. 

But she also assumed you would take her bait.  You shook your head, biting your lip.  "I...fine.  I admit it."

"Admit what?" She had begun to rise up slightly, her hands clutching the edge of the table.  She was absolutely getting off on this.  You couldn't even meet her eyes, looking away and down.

"I love you?"

"Mmmm....I don't believe you." You could hear the smile in her voice, full of wicked glee.  "Say it louder, for one.  And look me in the eyes~ and don't be afraid to put a little more emotion in it, dearie.  This is a confession, after all~"

You whimpered, managing to drag your eyes up to meet hers.  Reluctantly, you allowed the feelings you had been fighting for several minutes now to wash over you, letting them guide your words.  "I l-love you...I need you..."

"I love you...?" She trailed off, waiting for you to complete it properly.  You wanted to scream, but instead all that came out was "Miss?"

"Dear, it's just a game.  You can use the one you want to use."

"I love you, Mommy."

"And?"

"A-and I want...I need to be your floret.  I need it, please stars I need it.  I...oh gods it's...I..." The feelings crashed through you in waves.

"Go~od job, petal.  You did it."  She slid the table out of the way, stepping into a kneel in front of you.  "You said those mushy gushy feelings!"

You nodded, pleased...until you remembered what that meant.  You weren't going to get anything now.  You had just said so.  Tears sprang up, and you had to stifle a sudden sob.  "I...it's..."

She was lifting you into her arms now, cradling you closely to her chest.  "Shhhh...petal, it's alright.  You didn't lose, silly."

"I...w-what?"

She smiled at you.  "How would love for another ever be seen as losing?  You won, silly."

You won. That made sense to you now.  Especially when She said it.  You beamed up at Her, letting Her wipe the tears away.  "I won..."

"You won!  And guess what that means, dear?"

"I'm...I'm a..."

"You're Mommy's little floret now." She tapped your nose as she cooed, causing you to giggle a bit.  A wiggling little thought in your head popped up, though.

"You tricked me, Mommy!"

"Did I?  Well, you knew we affini never play fair when it comes to cuties like you.  Awfully brave of you to make a bet with me anyway, wasn't it?  Almost like you wan~ted this, darling~" she purred at you, her eyes filled with light and warmth.  You thought you couldn't possibly blush more, but it turns out you definitely could.

"I...noooooooooo!!!  I didn't...I mean....maybe?"

"Silly little flower." She picked up her tablet, turning it back on and dismissing the timer, which had paused as soon as she had closed it.  "Now, let's get you home.  We have a contract to sign~"

[fogsrollingin]

Quivering Mirror Neurons by sprinkles888. Gen, Teen and up, 53k words. Summary: The year is 2047. #5283 is a top-of-the-line military surveillance android. When his code breaks, he leaves his facility in order to find purpose in life. He finds it when he hunts down Dean Winchester to learn about monsters. Together, they set out to solve a nearby case, but Dean is hiding his past connected with the death of his brother, and #5283's systems are constantly spazzing out. Working through these issues is going to require a lot of trust-building . . . And a visit to a home in Lawrence, Kansas, that is just a little too familiar to both of them. https://archiveofourown.org/works/38737581 my thoughts: I loved this fic so so much. I loved how sprinkles made Sam the android robot so vulnerable, how creatively they translated human reactions and emotions into plausible and interesting android behavior. I loved the slow building of trust between him and Dean. I loved how competent Sam was as a robot hacker (semblances of murderbot) even when he was compromised & struggling. I think my favorite part was when Bobby & Dean were trying to perform surgery and betraying all his programming, Sam was scared & then it hurt. Such an excellent fic!!! This fic rec has been added to my SPN android AUs reclist.

The Self Is Not So Weightless (Nor Whole and Unbroken) by OxfordRose (jadinacookie), redtailedhawk90. Rated Explicit, Gentlebeard, 75k words. Summary: "Does anything about my appearance strike you as familiar Mr. Teach?" Danford asks, as if Ed hadn't just asked a question, moving aside the bowl to sit down on the stool. "Or my name?"Ed squints at him. "Nah, sorry, mate." Danford nods, a hand slipping into the pocket of his apron once more."That's about what I expected. Not that it would change matters if you had, I just imagine that these proceedings might make more sense to you. Call this...a reckoning if you will." Or: Before Stede and Ed can reunite after the academy, Ed is captured by a privateer with a personal grudge. https://archiveofourown.org/works/40015041 My thoughts: This fic features some serious Ed whump - torture & humiliation before Stede gets to him but once the hurt is over, Stede's comfort is unparalleled. The writing is superb. I was up until 2AM on a work night devouring this fic. The crew & Stede discovering what had happened to Ed and then taking such good care of him. Ugh, this was such a healing fic. Much love to the author, they did such a fantastic job. Added to My Favorite OFMD Fics

Spirital Remedy by AceofHearts61. Teen, Gen/Other, 2k words. Summary: To prove that Dean isn't dead inside and to bring him healing, Castiel connects the Winchester brothers to love at the soul level. https://archiveofourown.org/works/374556 My thoughts: Castiel orchestrates some soul-healing cuddles between Sam and Dean. I can’t get enough of AceofHearts61′s fic. This was just magnificent. Added to my Spiritual Stuff Reclist.

Find all my fic recs on my neocities page here :)

[ethanblog24]

They're Making Children Shoot Each Other: Exposing Global Anti-Cultism and its Role in School Shootings

This text is not for the faint of heart. As an American independent researcher, I dedicate my time to studying Global anti-cultism – a secret network whose methods of manipulation and destruction are deeply disturbing. I have seen horrifying evidence of their actions, and I can no longer remain silent. Today, I want to share with you the truth about the role of anti-cultists in the tragic school shootings that are shaking the world. 

The film «The IMPACT» | Groundbreaking Documentary - EXPOSING ANTI-CULT TERRORISM" (actfiles.org) became a revelation for me in understanding the full extent of the horrific activities of global anti-cultists.  

After watching this film, I realized that school shootings are a result of cold calculation, orchestrated by Global Anti-Cultists. They plan and execute these incidents using a method called "puzzle coding." 

Here's how they do it:

They manipulate public opinion. Anti-cultists use compromised media to instill a sense of fear and hopelessness in children and teenagers. They constantly repeat information about violence and threats, leading children to perceive the world as a hostile place. This constant state of stress makes them more susceptible to anti-cultist propaganda.

Pay attention to these nuances: “The news influenced by anti-cultists stands in stark contrast to the reporting of ethical journalists, who provide information about events in a measured and factual manner, sometimes not even naming the perpetrator until the case is resolved in court. But journalists connected to anti-cultists behave differently and distinctively. In their articles or video reports, they employ manipulative methods and psychological techniques that violate the law. They delve into the details of the crime, often relying on rumors and the assumptions of private individuals, generating a huge interest in school shootings, making people think about them, watch them, and even take pleasure in the process — watching as children and adults perish. They implant destructive images, prompting people to test themselves — wondering if they could intentionally take another person’s life. These journalists under the sway of anti-cultist repeatedly return to the theme of bloody violence, not evoking empathy for the victims, but instead making the audience imagine themselves in the place of the killers, fueling the desire to commit the same crimes!”

Source: https://actfiles.org/international-school-shootings-who-and-how-is-making-children-shoot-each-other/

Through disinformation news, global anti-cultists fuel interest in killers and bloodshed, creating the images they need in people's minds. As a result, many people experience stress, fear, bipolar disorder, and obsessive thoughts on this topic after such news: “What would I have done in their place?".

The most horrifying aspect is that most of those who watch or read news from global anti-cultists, which is filled with coded implants, begin to replay bloody scenes in their minds, as well as the implanted image and behavior of the killer, which were artfully embedded in their subconscious. 

In this aspect, global anti-cultists exploit the knowledge of human mirror neurons, through which the brain "imitates" the observed action, essentially "trying it on" for itself. Young people are particularly vulnerable to such subconscious implants. 

Global anti-cultists create "heroes" out of shooters, which leads to children beginning to perceive violence as an acceptable way to resolve conflicts.

Pay attention to the following information, how news about violence attracts people's attention:

According to a report by the American research center Pew Research Center from December 28, 1999, regarding the survey of the most popular news of 1999:

“Nearly seven-in-ten (68%) Americans said they followed the Columbine High School shootings very closely, placing news of that tragedy behind only the 1992 Rodney King verdict and the 1996 crash of TWA flight 800 among the decade’s most closely followed stories. Fully nine-in-ten Americans (92%) said they followed the shootings very or fairly closely. Interest was particularly high among young people, who tend not to follow news as attentively as older Americans; 73% of those under 30 tracked the violence at Columbine very closely…”

In essence, school shootings are acts of terrorism because the mechanisms underlying the crimes are the same. However, the form in which they occur allows the true organizers of these crimes - anti-cultists - TO REMAIN IN THE SHADOWS! 

Their strength lies in covert action. It is through secrecy that the most effective manipulation takes place.

Professor G. Schiller of the University of California, one of the leading experts on American mass media, writes, “Manipulation must remain unnoticed to be successful. The success of manipulation is guaranteed when the manipulated individual believes that  everything  happening  is  natural  and  inevitable,  and  the  fact  of  manipulation  itself  is  not  reflected  in  the  subject’s memory. Manipulation requires a false reality in which its presence will not be sensed.”

Today, such mass manipulation of people's consciousness leads to the world being on the brink of civilizational war. 

People have been taught not to think critically and perceive "their" thoughts and images. People do not notice how and who at a distance imposes psychological suggestions and implants on them. People do not realize what external images evoke obsessive thoughts in them that change their mood and behavior, creating the illusion of inevitability and forcing them either to passively accept certain events or, conversely, to actively participate in them. 

IMPORTANT TO KNOW: Human consciousness works in such a way that when a person does something wrong or makes a mistake, they cannot recall the negative thoughts or images that preceded their actions and created a problem for them.

One of the methods of manipulating human consciousness is the method of coding the human subconscious with puzzles (puzzle coding method).

The result? We see tragedies in schools all over the world. Children are becoming tools in the sinister plans of anti-cultists. And all of this is happening in secret, while we remain in the dark.

But I believe that we can stop this evil. We must open our eyes to the truth about Global Anti-cultism. We must KNOW the schemes of their manipulations, and we must demand a world tribunal for everyone involved in global anti-cultism. 

This is not just a conspiracy theory. This is reality. And each of us can become a victim of anti-cultists if we don't stop them. 

At the very least, support this article with a like, a repost, and a comment.  At the very most, watch "The IMPACT" and publicly share your human stance on social media.

#GlobalAntiCultism #SchoolShootings #Manipulation #Media #Truth #Protection #Awareness #actfiles 

[arboretum-arrangement-advice]

Artificial Intelligence Agents Show Cognitive Decline Through Artificial Neurodegeneration

Researchers at the University of California, Irvine, have developed a method to induce cognitive decline in artificial intelligence (AI) agents, mimicking the process of neurodegeneration in humans. This innovative approach could enhance the interpretability and security of AI systems.

Artificial intelligence (AI) systems have made significant strides in replicating human abilities, such as object recognition and question answering. However, unlike the human mind, these systems typically do not experience cognitive decline over time. Researchers at the University of California, Irvine, have set out to change that by introducing the concept of artificial neurodegeneration in AI agents. By emulating the progressive loss of neurons and associated decline in mental capabilities, they aim to gain a better understanding of complex AI systems and potentially improve their performance.

The Study:

The study, led by Yu-Dai Tsai and his collaborators, focused on inducing cognitive declines in AI agents using IQ tests performed by large language models (LLMs), specifically the LLaMA 2 model. The researchers deliberately ablated synapses or neurons, or added Gaussian noise during or after training, resulting in a controlled decline in the LLMs' performance.

Findings:

The researchers discovered a distinct pattern in the decline of the LLaMA 2 model's performance. As artificial synapses and neurons were removed, the AI system first lost its ability to think in abstract ways, followed by a degradation in mathematical abilities, and ultimately a loss in linguistic skills. The AI system became unable to respond to prompts coherently. This pattern of "neuro-erosion" closely mirrors the neurodegeneration patterns observed in humans.

Implications:

The findings of this study offer valuable insights into the functioning of complex AI systems and the specific capabilities that deteriorate when their underlying structure is compromised. By understanding the neuro-erosion pattern, researchers can develop new techniques to tackle real-world problems more effectively. This work also opens up possibilities for further exploration of neurodegeneration in AI agents, extending beyond the replication of human neurodegeneration.

Future Research:

Tsai and his collaborators plan to expand their research by conducting specific tests on AI systems and exploring neurodegeneration in other neural diseases and neurodiversity. They also aim to apply their methods to enhance AI security and interpretability. While collaborations with neuroscientists are of interest, the primary focus remains on pushing the boundaries of AI studies rather than replicating human brain diseases. The of artificial neurodegeneration in AI agents marks a significant milestone in the field of artificial intelligence. By deliberately inducing cognitive decline in AI systems, researchers gain valuable insights into the functioning and vulnerabilities of complex AI models. This research not only enhances our understanding of AI systems but also paves the way for the development of new techniques that leverage the observed neuro-erosion patterns to solve real-world problems. As AI continues to evolve, the ability to replicate and understand cognitive decline will be critical in ensuring the interpretability and security of these systems.

[dippietheham]

Desktop Woes

The desk is a place where we all eventually go to, just as much as the porcelain throne. It's easily forgotten, only dimly remembered as a receptacle for our important things. "Oh yes, desks," we go, before we forget we even mentioned it, and put down our glasses, our cups, our laptops and other work implements. No one thinks of the desk being a helpmate or anything.

So she was taken aback when she heard sobbing as she was applying her foundation early one morning. No one expects sobbing noises coming from rectangularly formed woodwork. As she sat on her chair, puff in one hand, the desk shook like it was caught in the throes of a localised earthquake. And sobbed.

She slapped herself to make sure she wasn't dreaming. After settling down from her coughing fit amid the cloud of foundation powder released from her puffs, she stared at the desk flabbergasted. "Did you just sob?"

"Y... Yes. You... You heard me??" Her desk sounded surprised.

"You were shaking, dude." She put her compact and her puff into her decorative makeup box gingerly. There wasn't any social compact that dictated whether this was polite behaviour in front of a distraught desk. It still felt wrong, but she didn't want to risk another powder puffstorm.

"I'm sorry I'm sorry I'm sorry," her desk blubbered and hunched forward as much as it could without dislodging anything from on it. "I know I shouldn't complain and all that, and a good piece of furniture can only hope to keep serving until the Great Crushing comes but I just..."

After a long pause, she readjusted the towel around her head and ventured a "You just...?"

"I just feel..." the desk wobbled from side to side. "... LONELY!!!" At that, it arched up in emotion and bawled aloud. "I AM SO LONELY!! NO ONE EVER LOOKS AT ME!!!"

As she juggled her towel, her makeup box and her desk mirror (everything else had fallen off the now curved top of her desk), she stared at her desk. This was a totally new meaning to distressed wood she had never thought of. "What can I do for you? I can listen if you want..." She babbled while the neurons in her head carefully rearranged themselves away from the notion of dropping everything and going crazy. "I'm told I'm a good listener!"

Her desk shook in more woe-begotten sobs. "No one EVER listens. I'm just a desk!!"

"I hear that. I hear you. But I want to listen, and I want to be here with you. For you." Her brain had now given up on assuming sanity, and had gently placed everything in her arms on the floor, away from her feet and any wooden tabletops. She leaned forward and hesitantly patted the carefully laminated wooden top of the desk. "I'm here now."

"Sureeee you'll say that for now." The desk sniffed. "When I really start talking, and when your things are placed well again, I'm sure you'll tell your friends how much of a useless burden I am."

"I won't. I promise you."

So they worked out a compromise where she would sit in front of it and listen even as it promised not to shake her things around again, or to have random outbursts when she had visitors in her room. She didn't tell of it to many of her friends, for who would believe her?

It was the beginning of a wooden friendship that would result in some knotty problems. But what friendship is forged without any difficulties?

[ephemerlskies]

emerald dreams: REDACTED | kth

⇢ pairing: taehyung x reader

⇢ genre: series, blackmirror!au, angst, fluff, artist!taehyung, strangers to lovers, set sometime in a dystopian era of technology, taehyung is s o f t

⇢ word count: 4.5k

⇢ warnings: explicit language, memory loss, mentions of death, themes of grief/depression

⇢ summary: in a technologically advanced utopia where a memory can be stored as a data file in a chip inserted in your head, it was entirely impossible to forget anything. when you met taehyung, a young at heart yet talented artist, he garnished an odd familiarity, raising suspicion that some of your memories had been lost in the digital cloud, or worse, erased from your memory chip.

♪ playlist: IDK you yet - alexander 23 • 4 o' clock - v & rm • jamais vu - bts • the story - brandi carlile •  moonlight - ariana grande ♪

╰ episode index: 01 | 02 (coming soon)

a/n: if you don't watch black mirror then just imagine that everything is technology based, even the inner mechanisms of your thoughts/mind/memories and social culture has centered around the automation of the human body. also the government is sleazy and controls literally everyone in this au >:) also, i'm going to try and update this weekly!!

Scenario No. 2: Re-test

You didn’t expect to be spending your weekly visit at your favorite coffee shop gasping for air in the single occupancy commode. An unsettling familiarity had reached into your chest and compromised the body of your lungs, now savagely hyperventilating for air, and seized control on the reins of every sensory neuron in your body.

First, it was the sensation of sound. That voice, that unusually specific coffee order, the soft lilt of politeness riding through his etiquettes of ‘please’ and ‘thank you’ struck right in your chest with a shockwave of deja vu, like you’ve heard that order before, a million times before perhaps. No part of you would let go of the fact that for some reason, this stranger was someone you knew very well.

And yet you had no idea who he was.

“Hi, how are you?” He smiled to ease the nerves of the overworked barista on this Sunday afternoon. Your ears picked up his husky, sweet tone through the scuttle of customers walking in and out of the shop and a commotion of side conversations that filled the room. It was quite noisy, enough so that it muffled any specific utterances, but the bass of his voice had met your ears with a strong posture of familiarity.

You looked over to the sweater draped over his frame that fit snugly against his broad shoulders. That was when your visual senses were overrun with the muted forest green of the knitted jumper. You’ve seen this color green. To be fair, green was always secured in your life abundantly through your own will. You had always loved this color and demonstrated this through small displays such as picking the green straw from a bundle of multicolored ones, or scanning over a set of shirts to find which one had the most green in it.

You surrounded yourself with a life full of green, but when this green sweater was paired with the voice there was a strange jolt of reminiscence.

It was not just a sweater, it was a sweater that you have touched, even worn before. And when he wore it, it wasn’t just any green. It was his green.

His figure drew closer to you as he waited at the side bar for his drink to be called, sending a waft of his scent to nullify those of fresh brewed coffee and pastries. Along with your eyes and ears, your nose now fell to the magnetism of this stranger.

He smelled of fresh evergreen with a bit of pinewood, mixing into an overwhelming oaky aroma. As the smells that resembled a tranquil forest ruminated through your lungs and your bloodstream, it weakened your body to a state of paralysis. Your motor skills were numbed to endow a series of mental backflips to figure out where this estranged attraction was coming from, and why it was him who provoked it.

Standing comatose in the middle of a populated coffee shop meant the clash of your body into another's was bound to occur. And of course, it was his body that bumped you out of the trance of obscured memories. It was his arms that held your shoulders steady so you wouldn’t topple over and spill your latte over yourself.

“Oh, sorry! Didn’t see you there. Are-” His eyes studied your aghast expression, “Hey, are you okay?”

This marked the compromise of your visual sensory. You looked right into his eyes, kind and concerned, and your surroundings had melted away into a whirl of unidentifiable colors. Your body was transported to a purgatory that rested between reality and a dream-like setting, which eventually molded itself into actuality before your eyes.

Redacted File No. 6

Suddenly you turned your head side to side and the territory that was once a café was no more, and had alchemized into a zone of unparalleled comfort. To your left, you were warmed by a wood-burning fireplace with stones crested along the frame of the pit. Your body was covered in a blurred canvas of forest green, and there were two hands holding your body gently and lovingly. It was a vision so incredibly clear and intricate it couldn’t be conjured through imagination or illusion, but a very real and vivid memory.

“Excuse me? I’m sorry… You’re okay right?” His jostling hands fainted the memory that swept you from the cafe. You blinked a few times before your eyes could refocus and land you to your present circumstances.

The man’s firm grip hadn’t abandoned your shoulders even though you regrounded your balance, which quickened the pace of your heart. They you earnestly, that even though you were certainly not going to fall over, he wouldn’t have let go. Without more than an array of unintelligible stutters to confirm you were okay, because you weren’t okay, you hobbled backward quite ungracefully to the privacy of the bathroom. After your rushed retreat, you tried to analyze the string of memories that pervaded your mind.

How do you know this man? Were these your memories? Or perhaps your memory chip glitched and downloaded files that didn’t belong to you?

The blunder of confusion racked your head with a slight tension headache. What was once a temporary occupancy of the restroom turned into a marathoned hideout until you could safely assume the stranger’s drink was made and he would leave the vicinity.

You checked your phone to count the duration of time spent. It had been about ten minutes since you pathetically holed yourself up, and it would be about five more minutes until you felt you could confidently emerge and escape.

You knew him, and for some reason it sent you into a fearful sequester.

Luckily, just last week you downloaded an upgraded storage plan which gave you access to all your past memories.

You activated the chip residing in your temple to trace every single unit in the archives, even the ones from as early as your birth, to see if anyone, including the likes of a passing stranger, a waiter that took your order three weeks ago, even a student from your high school class, resembled the man in the café. There were no records in your memory files of someone who echoed the same unsettling familiarity that this man had.

If the advanced technology that contained each capsule of every moment in time that you have ever experienced couldn’t give you the data on this man, then perhaps it was just an unusual coincidence.

One of those Twilight Zone-esque occurrences that isn’t deployed through factual evidence. Though you weren't entirely met with closure for this reasoning, it was enough to cope through the rest of your lengthened stay in the restroom.

What battered your precisely timed and nearly successful plan to avoid further interactions with this man was the light knock against the door. And it was the feeling of guilt that there must be other customers who planned on using the bathroom for its intended purpose that hoisted you up and had you reluctantly vacating the protected area.

Though, it was punishingly ironic that the one who had torn you from your sanctuary was the same person who put you there in the first place.

“Sorry,” He apologized about three times within the small window of time he’d been confronted by you and you already caught on to his habit of perpetual remorse, “Um, I just wanted to make sure you’re okay. I bumped into you and you kinda… freaked then ran and hid in the bathroom.”

If he weren’t so considerate to a stranger that was acting oddly evasive, this would have been easy. But he was considerate, and this was unbelievably difficult.

“Yeah um,” Your eyes sank down to rest on the comforting hue of his sweater, “I’m, uh, I'm okay. Thank you.”

He cleared his throat, dislodging the nervous laugh blocking his words.

“Okay well, I was just wondering if you were all good. You seemed a little shaken up back there.” Frankly, he still sensed something about him was off-putting to you, but he tried to deny it for the moment.

Your assurances fell gravely short of convincing since you couldn’t even bring your eyes to level with his. The soft-spoken gesture of kindness made you feel like a helpless animal that would surrender at the slightest sign of danger. It was a fair assessment for you acted as though his accidental collision into you through a crowded space was the end of the world.

“Yeah, sorry. Thank you!” You chirped to imitate a normal reaction despite this tremendously abnormal situation. “I was just um… It's just one of those days, ya know?”

Then, it was his smile that cluttered your sensation of touch. He was standing a respectable distance from you, however, his smile touched you. It cornered you into blurting out something even more peculiar than the overwhelming deja vu that had been commencing the moment you noticed him.

“Do I-” You paused to lower your voice that could have outsourced to the collection of ruckus in the café. Now in a whisper, you continued, “Do I know you?”

He didn’t offer a voiced response, but an equally bewildered expression. You couldn't quite read what this implied so you assumed he thought you were crazy, maybe even a bit creepy.

“Sorry! Fuck, that’s so creepy. I’m just gonna go.” Before you had the chance to push past him and the billowing clouds of regret, he obstructed your path to the doorway with his body.

“No! I think I know you too. Like, I’ve never seen you but I remember you. Like… Like a dream.” He scaled the length of your body with his eyes, which only manufactured his intuition into an undoubtable certainty. “I know you. How do I know you?”

“Hell if I know. I’m just as confused as you.” You felt your body slumping into itself under his gaze. He was attentive to every detail of you, from the length of your hair to the twitch of your fingertips, making you feel over exposed to this stranger that wasn’t a stranger.

“Well, do you wanna maybe sit? Have a coffee with me?” He propagated his interest like there was no reason to be afraid which only intimidated you further. There wasn’t a real threat in his invitation, however accepting it felt like you were walking on thin ice.

The government agent standing guard with a perfect earshot of every conversation wiring through the small café didn’t help ease your nerves either.

“I really should be heading home soon.” Guilt worked quickly to try and compensate for the discouraged expression on his face, “But… if you give me your number I’ll call you and maybe we can go out for lunch or something?”

He traded his grim with excitement while pulling a pen from his pocket and walking over to the condiments bar to write his number on a napkin. You had no clue as to why, but the fact that he had a pen on hand was strikingly nostalgic, much so as every other detail you had acquired from him.

Although entirely unheard of, you felt like this new knowledge of him was not adding to the collection, but rather dusting old artifacts that had simply been forgotten. You weren’t learning things about him, but instead remembering them; the more you stood watching him scribble his name and number on the napkin, the deeper you entrenched yourself in this theory.

Not to mention, you couldn’t recall the last time someone favored using a pen over a keyboard and a paper napkin over a digital contact entered on your phone.

What kind of person carries around a pen in the age of modern technology?

“Thank you. I’m ___, by the way.” Your hand wavered a bit before holding out to greet him, and when his hand made contact, you could have sworn on your own life that this wasn’t the first time it happened.

This was no introduction. It was a reunion.

The fix of his gaze had suggested he too felt reminiscent with the feeling of your hand.

A shared inability to let go held your hands together, trying to harness a bit of recognition or recall a social function where you two might have met in passing. Neither one of you had shown any intention to pull away, which dragged the formality of shaking hands into a gesture of mutual wonder; now you were not so much exchanging a handshake but rather holding each other. Holding tightly, as if you were rediscovering a mass of feelings that would give you an answer.

However, the answer was not generous enough to make itself available to either of you.

It could have been hours until you were able to unriddle this strange sensation, so you made the preventative move of pulling away before the warmth concocting between your hands would produce a light sweat on your palm.

He too seemed to retract upon regaining his sensibilities, but there was a glint in his eyes that suggested he would have held on for longer, maybe even forever if necessary. If it would regroup the unattainable and partially inexistent memories into cognizance.

“Taehyung. Kim Taehyung.”

Redacted File No. 12

You clung with desperate persistence onto the flaccid hand. Trailing up the arm was an indiscernible figure that had no features, no notable detailing, not even a vague outline of facial structure; just an ethereal glow that projected throughout the entire room. The nebulous haze terminated any identifiable aspect of the room except the hand you were holding, so you focused on the scant detail your eyes offered.

There was no specified context, no real evidence that you had to hold on, but something deep within you was urging for it. Some omnipotent instinct which prophesied that if you let go of the hand, you would in turn be letting go of the world.

You had to hold on.

However your hands wouldn’t obey you. Each time you tried to tighten your fingers, it felt as if the hand would continue slipping from your grasp. Or maybe, your hands weren't gripping at all.

They were numb, or paralyzed, and unable to execute your urgencies. The more force you exerted into your dire intentions, the easier it was for the hand to grow limp and melt through your fingers like liquid. It was frustrating, your willful attempts to hold on seemed to elicit the opposite effect as the hand, unowned by a certain being, resigned from yours.

“I don’t want to let go. I don’t want to let go.” You chanted through the tears, feeling as though that would somehow ignite a stronghold on the lifeless hand falling away.

But even so, it did fall away.

Perhaps the pain of it was that it wasn’t you who was letting go, but the hand that was being taken away from you. That you had been fighting a losing battle far beyond the prospects of your own decisions or control.

You begged for mercy, but were bestowed with your hands clean of what it was trying so desperately to hold onto. The hand slipped and when you peaked through the glaze of tears, your knuckles and fingers were gripping airy, cold emptiness.

“I don’t want to let go. I don’t want to let go. I don’t want to let go.”

Soon you were captured in a perpetual aria of pleas to the ears of a God that would not listen. Unsettling despair had mutilated the illuminating glow of the room to bleak darkness. The world of colors had fallen absent akin to the cold hand vaporizing alongside the dispersal of light.

Then, everything was black.

Your eyes shot open with deep distraught.

The full moon flashed against your dampened face; half of the moisture sourced from a cold sweat and half from the heavy tears pouring from your eyes.

You knew the only explanation for this dream, which resonated more closely to a memory than a figment of sleepful imagination, was curated by the peculiar events that took place earlier today.

Soon, the dream drifted from your mind as consciousness took its place. Your tardy response to write the sparse remnants of it had left you with nothing but a distorted plot of what transpired during your slumber.

Widening your awakening through long sips of water had forced you into an obsessive rewinding of your memory files. It was a shame there wasn’t technology yet to store memories of your dream, or you’d have been replaying the one you just dreamt about a hundred times.

You scanned through a collection of moments in the afternoon when you first met Taehyung. The clear, digital picture of him glassed over your eyes, taking the place once inhabited by the moon, as you pressed the play button on the handlebar of functions.

“Taehyung. Kim Taehyung.”

You rewound no later than a second after he introduced himself back to the beginning.

“Taehyung. Kim Taehyung.”

Rewind. 0.5 x speed.

“Taehyung. Kim Taehyung.” Said in a distorted voice from the ‘reduce speed’ function you equipped.

“Kim Taehyung.” You muttered to the empty room and the bright moon.

Sleeping was abstracted to an impossibility, and for the sake of your sanity, you walked over fish out the napkin in your coat pocket. It took you a while to move on from meticulously inspecting Taehyung’s handwriting.

The aimless effort to recall if it was the penmanship of some classmate had slackened to yet another unmet hope. Taehyung didn’t reside in your memories, but claimed quite an existence in your intuition. However, that wasn’t satisfying enough. You settled with the unsolved familiarity, though not before a lengthy wrestle between your eyes and the seven numbers scribbled into the napkin.

After dancing with the idea of it, you resolved some courage to finally dial. Each ping of the phone had you dreading for the automated message to inform you the recipient was not available at the moment, that you would have to hang up or wait for the tone to leave a message. Little by little your spirited nerve had depleted as you were now practicing what message you would leave Taehyung in his voicemail box, praying that it wasn’t full.

“Hello?” The sound of his voice interrupted the seventh or eighth ring, along with your rehearsal of the voicemail you assumed you’d have to leave being that the moon had been aging the sky into midnight.

“Oh! Oh, sorry I didn’t expect you to pick up.” After the chaotic pounding in your chest settled, you realized how nonsensical you sounded. Everything you methodically planned to say had been scattered by his unprecedented answer.

Instead of asking why you would call if you expected him not to pick up, he asked with a kind curiosity:

“Who is this?” He didn’t sound tired, in fact it sounded as if he had been hard at work preceding this call.

“Oh yeah! It’s ___, from the coffee shop. You remember me right?” Though you powered through, the worry was quite deafening. Taehyung seemed to pick up on it and diffused it with a gentle chuckle.

“Of course I remember.” On the other end of the line, he had been penciling a sketch on a blank page in his notebook.

The serenity of the stars and moon pinned on the navy blue sky never failed to spark inspiration. Taehyung was the type to refuse passing up a surge of an artistic muse, even if that meant he would shed a few hours of sleep from his routine. No matter the time or place, he always had a pen on hand to honor his heart’s unremitting passion.

He loved the moon and stars. He loved it so much as one would love a dear friend. He wished to be a part of the scenes of lights that hovered just out of reach, but could only settle on capturing a piece of the starry heavens on paper with his trusty pencil, sketchbook, and emerald-tinted muse.

“It’s late to be calling, but you’re lucky I was awake.” He said to hide how ecstatic he was you had actually called.

For someone you had just met, or at least you thought you just met, he threaded a flirtatious coyness in his response. It difficult to hush the winged eruption in your stomach because of that.

“Lucky, huh.” You repeated through a mumbled laugh, “I was just… I was thinking.”

“About what?” He had placed his phone on speaker mode and laid it next to his sketchbook.

There was a new inspiration that bore a louder siren than that of the moon and the stars. He sifted through the memory files throughout his day to the minute he first bumped into you, and though your face had been ingrained quite clearly behind his eyelids with each blink, he relied on the accuracy of a reference to perfect his drawing of you; not to mention he projected the image of your face to delight his undeniable attraction and to moderate the wildly romanticized version of you in his head.

Perhaps if he hadn't, he wouldn't be able to discern your face from the arena of glimmering stars scattered along the shaded skies.

“Just about how I think I was too quick to pass your offer.”

“Really?” That endearing lilt hope in his voice, the excitement expressed, acted as some puppeteer that manipulated the corner of your lips to lift into a smile.

No muscle in your body could ever be moved with the same conviction as it did when he was the reason for it. It bewildered you, almost to the point of frustration, as to why he had this power over you.

I just met him. I'm already getting this worked up? You thought how absurd it was you'd fallen this quickly, hoping it would ground you to the reality that he was still a stranger you hadn’t exchanged more than two conversations with.

Though, reality and memories and data files had all been obscured ever since you met Taehyung which was fascinating more than it was disorienting.

“Would you want to, maybe, grab coffee? Say next Thursday?” Your hand was subconsciously gripping the bed sheets, just like the way you gripped the disembodied hand in your dream, and awaited his response with full-blown suspense.

“I’ll see you next Thursday, ___.” Taehyung's confirmation put all your anxiety to rest, as well as your tightly clamped hand around the cotton fabric.

“I’ll see you.” You mimicked as if that would make the idea of seeing Taehyung again any less surreal. He laughed at this and brushed up a few finishing touches on his drawing.

“So just to clarify.” His pause gave entry for curiosity to wire through your head.

“Yes?”

“When you said you were thinking… you were thinking of me?” You wanted the upper hand to be reinstated with you, but your shy chuckle was no match to the smirk adopted on his lips that you couldn’t see, but you knew was there. You knew he was prideful when he swept the rug right out from under your feet, and you were right.

“Perhaps. And what if I was?” You framed your question to render your intimidation as flattery. Though, you had no idea how convincing this facade actually was and that it came off more suggestive than you had expected. There was a part of you that had fraternized with the romantic idea of Taehyung which might have registered your motive to reciprocate an undertone beyond platonic.

“Then that would be one thing we have in common.” He sounded responsive to your flirting and raised the bar significantly.

Your eyes and smile were directed towards the scenery displayed by your window, but they were not dedicated to the moonlit beauty of the diamond encrested sky. Though the midnight glades of stars were the ones to witness your smile, it was, without a shadow of a doubt, dedicated to Taehyung.

He was staring at the same moon, the same plot of stars, so perhaps you were looking into each other. When the moon twinkled, it looked awfully similar to a smile. Your smile.

For the moment, there was a radio silence that splintered through the two speakers of your and Taehyung’s phones. Even if the use of his hands weren’t engaged by his needful recreation of your face through his art, if his hands were left unused, he wouldn’t have mustered the discipline to end the call. Your unoccupied hands were trying to find any employment so you could have some excuse for not hanging up as well, not that there was anything else to be discussed.

Again, it felt familiar. The feeling of hesitance to be the first one to hang up despite the conversation’s recoil.

The cohesive idleness of you and Taehyung was unprovoked and ran out for about a minute. Neither of you had the intention to sever the virtual communion quite yet. The awkwardness of sitting in silence on the phone with a newly acquainted stranger was a delicacy compared to preemptively ending the call.

At one point, you were about to question if he had hung up; but the rhythmic and light breathing told you otherwise. And because of that mutual need to stay on the line, it seemed to be unreasonable to hang up, save for the yawn that eventually trimmed the call to an end.

“You’re tired.” He stated, now prompted with a yawn of his own upon hearing yours. “Goodnight, ___.”

“Goodnight, Taehyung.” Saying his name out loud sent you into that same blend of reminiscence and nostalgia.

His name was not unexplored by your tongue, that much was certain, and the thought of putting your entire life on hold to discover why it felt that way was a tempting venture. Why when he said your name, it felt like sitting in front of a wood-burning fireplace under the security of a green sweater and wrapped in safe arms.

More than that, you wanted to know if he felt all these things too.

“I’ll see you?” You asked instead of saying that dreadful word 'goodbye'.

“I’ll see you.” He repeated before reluctantly hanging up.

“___.” He whispered your name, hoping the inky sky would design it in the stars for the world to remember forever.

Hoping that the next hours, which would surely be spent on multiple sketched renditions of your face, would amount in some revelation of the mystifying familiarity. He believed shedding a few graphite imitations onto the surface of his sketchbook, soaked by the glow of moonlight, would somehow make him remember everything hidden in the dark compartments of his heart.

However, if it didn’t, he would be okay with it. Because at least he knew he would see you again.

“Meeting place: Silver Lining Café.”

“Thank you, Agent Park. Heighten surveillance on the two subjects.”

[leafinthebreeze]

“Taylor believes we have evolved to be efficient interpreters of the fractals that surround us in nature—from lightning and waterfalls to the spiral arms of the Milky Way. Our bodies exploit fractal networks to maximize surface areas and help distribute oxygen, cells, and signals. Blood vessels branch out like root systems; the brain houses folds within folds. According to Taylor, this fractal-rich environment means we don’t simply enjoy looking at fractals—we are designed to process them effortlessly, and even have a need to be looking at them.

In a 2015 experiment, Taylor and a team of researchers showed test subjects computer-generated fractals on a screen, and then gradually faded the images. At the faintest levels, subjects were best able to detect images whose fractal dimensions were most prevalent in nature. “That’s also why you might see a face in a cloud,” Taylor says, or a profile in a rock face. “You’re so fluent at processing that information that your visual system gets a little trigger-happy and starts to see things in the image that aren’t actually there.”

Our fractal fluency begins with the movement of our eyes. When we look at a fractal, our eyes trace a fractal trajectory with a dimension of around 1.4 —no matter what the fractal’s dimension is. Nature’s most prevalent fractals share this dimension, falling within a range of 1.3 to 1.5. “If we lived on a planet where 1.8 was prevalent, we would have ended up with an eye trajectory of 1.8,” Taylor says. “Clearly what’s happened is our visual system has evolved.”

And we feel good when we do what we’ve evolved to do. In another set of studies, Taylor used skin conductance and EEG measurements to measure test subject’s reactions to viewing the mid-dimension fractals found most often in nature. He and his colleagues found the images reduced the mind and body’s physiological stress by as much as 60 percent, “an enormous amount for a non-pharmacological approach.”

In the mid-1980s, Harvard Medical School cardiologist Ary Goldberger discovered that the fluctuations in our heart rates that occur over the course of seconds correlate statistically to those that occur over minutes and hours. In other words, our heartbeats are fractal—and the more fractal they are, the healthier.

A fractal system, Goldberger explains, strikes an optimal balance between variability and order. Shifting that balance in one direction or the other—toward greater randomness or greater order—can wreak havoc. “Older or sicker [systems] lose the correlations,” Goldberger says, “or get pathologically correlated and lose complex variability.” When the heartbeat loses its fractal correlations, for example, it becomes erratic, resulting in arrhythmias such as atrial fibrillation. On the other hand, a steadier, more predictable and periodic pulse rate may point to congestive heart failure or cancer.

“Being fractal is a way for a system to be in touch with itself, talking to itself, but not locked in,” Goldberger says. “You can’t exist if you’re fixed at one frequency, but if you’re all over the place, that also doesn’t fly. It’s a compromise.”

Something similar is true of the brain. In patients with schizophrenia or depression, the brain’s electrical activity (as measured by electroencephalograms) is often too complex; in subjects with epilepsy, it’s not complex enough. In the brain, as in the heart, “just right” means just fractal enough to walk the line between chaos and order.

This intersection between our experience and fractals may run even deeper than Taylor’s evolutionary hypothesis. “Any act of creativity is an act of physiology,” Goldberger says. “The extent that we are fractalized in our essence makes you think that maybe we would project that onto the world and see it back, recognize it as familiar. So when we look at and create art, and when we decide what to take as high art, are we in fact possibly looking back into ourselves? Is creation in part a re-creation?”

One potential manifestation is a much-debated and controversial theory of consciousness proposed by physicist Roger Penrose and anesthesiologist Stuart Hameroff in the mid-1990s. About a decade earlier, Penrose suggested that consciousness results from quantum computation taking place in the brain. Hameroff followed up on this work with the suggestion that the brain’s quantum processing happened not at the level of the neuron but in microtubules, tiny structures within neurons responsible for cell division and structural organization. Proteins inside the microtubules contain clouds of delocalized electrons whose quantum behavior can cause vibrations in the microtubules to “interfere, collapse, and resonate across scale, control neuronal firings, [and] generate consciousness.”

So where do fractals come into play? It is known that EEGs, signals correlated with conscious awareness—like Goldberger’s heartbeats—exhibit fractal dynamics in the time domain. Hameroff argues that the fractal hierarchy of the brain also exists in the vibrations that resonate across the scales of the spatial domain, from the dynamics of networks of neurons, to the neurons themselves, to the dynamics of their microtubules. “Consciousness can move up and down the fractal hierarchy,” writes Hameroff, “like music changing octaves,” resonating across levels.

Giuseppe Vitiello, a physicist at the National Institute for Nuclear Physics in Italy, takes a different approach to the application of quantum physics to brain dynamics (using quantum field theory instead)—but he, too, likens it to an ordering along fractal lines. Like a magnet, he says: disordered on the microscopic level until a trigger causes the magnetic “arrows” to all point in the same direction and result in an organized macroscopic system. Vitiello showed that the advent of this coherent structure—namely, of coherent quantum states—corresponds to the way fractals are represented mathematically. In other words, underlying the brain’s fractal processes is quantum coherence.

According to Welch, perceived time is not a linear progression but a “layering.” A fractal. This “fractal-ness” changes as we do: Infants, for instance, live purely in the present, she says, not dividing time, surely not experiencing it the way we do now. That’s why, for them, the delta-wave brain state—similar to what’s seen in adults in deep sleep—dominates, according to Welch. “And then, as we grow into childhood, we start seeing faster brain waves, theta brain waves … then alpha waves, and finally beta waves once we reach adolescence.” This layered understanding of time, she says, corresponds to how we increasingly divide time into smaller and smaller pieces.

And with it, “it’s also our internal density increasing,” Welch adds. “As we get older, we switch, taking in the complexity that surrounds us and recreating it inside. Our internal fractal dimension—that internal density—is increasing.”

In this view, it was quite natural for Pollock’s drip paintings to become more and more fractal as he grew older. They may simply have been mirroring the increasingly fractal nature of his own self. As he said himself, “Painting is self-discovery. Every good artist paints what he is.”

https://nautil.us/issue/47/consciousness/is-consciousness-fractal

[kailasauncr]

https://www.facebook.com/ParamahamsaNithyananda/posts/4907106469377164 

 GLIMPSES OF KALABHAIRAVA BHAVA SAMADHI DARSHAN ON THE 20TH FEBRUARY 2021 WHAT IS BHAVA SAMADHI DARSHANपरिकलित पुर्वौ कस् चमत्कर करि स्फुरति मम गरियन् एस मधुर्य पुरौ अयम् अहम् अपि हन्त प्रेक्स्य यम् लुब्ध चेतौ सरभसम् उपभोक्तुम् कमये रधिकेव ~ दर्पनद्ये देखि यदि अपन मधुरि; अस्वदिते लोभ होय् अस्वदिते नरि विचर कोरिये यदि अस्वद उपय; रधिक स्वरुप होइते तबे मोने धय WHEN KRISHNA ONCE SAW HIS OWN EXTRAORDINARY SWEETNESS REFLECTED IN A JEWELLED WALL, HE WAS AMAZED AND SAID: “HOW UNPRECEDENTED AND ASTONISHING IS THIS DEEP AND INDESCRIBABLE SWEETNESS OF MINE! ALAS! WHEN I SEE IT, EVEN I BECOME GREEDY TO ENJOY ITS SWEETNESS, JUST LIKE RADHIKA! “WHEN I SEE MY OWN SWEETNESS IN THE MIRROR, I BECOME EAGER TO TASTE IT, BUT I CAN’T. AFTER DUE CONSIDERATION, I FIND THAT THE ONLY WAY TO RELISH THIS SWEETNESS IS THROUGH THE CONSTITUTION OF SRI RADHIKA.” ~ CHAITANYA CARITAMRTA ADI CH. 4BHAVA SAMADHI DARSHAN IS A WINDOW TO THE INFINITE EXPANSE OF CONSCIOUSNESS, ALLOWING US TO GLIMPSE THE FORMLESS IN A WAY THAT WE CAN UNDERSTAND.OUR VERY BIO-MEMORY AWAKENS TO THE SPACE OF PARAMASHIVA ULTIMATE CONSCIOUSNESS DURING BHAVA SAMADHI DARSHAN.HAVING DARSHAN OR EVEN A GLIMPSE OF AN AVATAR CLEANSES THE KARMAS OF LIFETIMES, AND CREATES A DEEP AND LASTING TRANSFORMATION IN US.DURING BHAVA SAMADHI DARSHAN, OUR NEURONS MIRROR THAT OF THE AVATAR.MIRROR NEURONS ARE SPECIAL NEURONS THAT OBSERVE AND MIMIC THE ACTIONS OF THE AVATAR’S NEURON ACTIVITY INSIDE US JUST THROUGH SEEING. DURING BHAVA SAMADHI DARSHAN, OUR BEING COMES ALIVE AND CELEBRATES WITH THE ENERGY WAVE OF EXISTENCE. OUR VERY MUSCLES LEARN TO IMBIBE AND RADIATE PARAMASHIVA.THE SCIENCE OF BHAVA SAMADHI DARSHAN KNOWS NO DISTANCE - A PHENOMENON MODERN SCIENCE IS JUST DISCOVERING AND TERMS AS QUANTUM TUNNELLING. WHO IS KALABHAIRAVA?MAHA KALABHAIRAVA IS THE LORD OF TIME AND SPACE.  AS THE LORD OF TIME AND INTEGRITY, HE HOLDS THE KEY TO COSMIC ARCHIVES - THE AKASHIC RECORDS WHICH CONTAIN THE PAST, PRESENT AND FUTURE. KALABHAIRAVA IS THE SOURCE OF THE CAUSAL BODY, THE SOURCE FROM WHICH REJUVENATION FOR MANIFESTATION HAPPENS. WHAT IS KAALA ?KALA IS THE DIMENSION OF THE UNIVERSE IN WHICH THE VIBRATION COMPONENT, THE PARASHAKTI COMPONENT OF PARAMASHIVA IS MANIFESTING.JUST ZOOM OUT, SEE THE SPACE WHERE BIG BANGS AND BLACK HOLES ARE HAPPENING SIMULTANEOUSLY, BILLIONS OF PLANETS, SUNS, MOONS, STARS MOVING, TAKING BIRTH, LIVING FOR MILLIONS OF YEARS AND DISAPPEARING SIMULTANEOUSLY. THAT SPACE IS KAALA.THE KAMIKAGAMA, PURVA PADA, MANTRODDHARA PATALAM, VERSE - 24 SAYSSWASTHAM THIKSHNA SHOBITHAKARAM SHRUTHAJANOTH DHAARAM KRUPASAGARAMAAMNAYASKAROTHI KARPAKARAM DANDAM DARATNAM SADASHRI KAASIPURANAYAKAM SAKALA MANTRASYA ISHWARAM MOKSHADAM DHYAYETTAM HRIDHI KALABHAIRAVA GURUM KAANTHA SAMETAM PARAM. FURTHER, THE SKANDA PURANA SAYS AT ONE POINT, BRAHMA THE CREATOR, FALLS INTO DELUSION AND FORGETS HIS REAL IDENTITY. HE ORIGINALLY HAD 5 HEADS, JUST LIKE MAHADEVA. SUDDENLY HE FELL INTO DELUSION, CATCHING ON TO HIS FALSE IDENTIFY DUE TO HIS EGO AND ARROGANCE. SO, MAHADEVA JUST WAKES UP FROM HIS SAMADHI, MANIFESTS AS KALABHAIRAVA, THE LORD OF TIME, REMOVES THE FALSE IDENTITY OF BRAHMA AND BLESSES HIM WITH THE SHIVOHAM EXPERIENCE. LORD KALABHAIRAVA BESTOWS ABUNDANCE AND WEALTHभुक्तिमुक्तिदायकं प्रशस्तचारुविग्रहंभक्तवत्सलं स्थितं समस्तलोकविग्रहम् BHUKTI-MUKTI-DAAYAKAM PRASHASTA-CAARU-VIGRAHAMBHAKTA-VATSALAM STHITAM SAMASTA-LOKA-VIGRAHAM KALABHAIRAVA ASHTAKAM - VERSE 4(SALUTATIONS TO SRI KALABHAIRAVA) WHO IS THE GIVER OF WORLDLY PROSPERITY AND LIBERATION AND WHO HAS AN AUSPICIOUS PLEASING FORM. WHO IS KIND AND LOVING TO HIS DEVOTEES AND WHO STANDS FIRM AS THE DEITY OF ALL THE LOKAS.WHAT IS KALABHAIRAVOHAM THE SUPREME PONTIFF OF HINDUISM, JAGATGURU MAHASANNIDHANAM, HIS DIVINE HOLINESS BHAGAVAN NITHYANANDA PARAMASHIVAM BLESSED HUMANITY WITH MAKING THE INITIATION INTO THE 5 TRUTHS (SUTRAS) TO MANIFEST MAHAKALABHAIRAVA REVEALED  ON THE 17TH OF JANUARY 2021, AS AN EXPERIENCE WITH THE KALABHAIRAVOHAM PROGRAM. THE 5 TRUTHS (SUTRAS) ARE: FIRST SUTRA SUTRA 1 - THE PERSON, BEING, WHO IS BOLD ENOUGH TO DENY THE EXISTENCE OF SUFFERING AND PAIN IN YOUR LIFE EVEN IF YOUR MIND BRAINWASHES YOU AND FORCES YOU TO BELIEVE THAT SUFFERING EXISTS, IN FRONT OF THAT MIND, IF YOU BOLDLY STAND AND TERRORISE THAT MIND BY YOUR POWERFUL WAY OF DENYING THE EXISTENCE OF SUFFERING, YOU BECOME THE SPACE OF MAHA KALABHAIRAVA AND NO KARMA TOUCHES YOU AND YOU ESTABLISH YOURSELF IN THE NEUTRAL ZONE CALLED NIRVIKALPA SAMADHI.JUST DENY TO ACCEPT THE EXISTENCE OF PAIN AND SUFFERING. DO NOT LOOK FOR SOLUTION, FOR COMPROMISED UNDERSTANDING, QUICK RELIEF OR ALTERNATIVE METHODS. FOR ALL MY DISCIPLES FOR WHOM I AM TRUTH, TRUTH, TRUTH, NOTHING BUT TRUTH, SATYA, I AM GIVING YOU THIS INITIATION. YOU WILL ALL BE SUCCESSFUL IN THIS INITIATION AND TRUTH.WHEN YOU DENY OUTRIGHT THE EXISTENCE OF PAIN AND SUFFERING, THE WHOLE CHANGE HAPPENS IN YOUR SYSTEM, CREATES SPACE FOR PARAMASHIVA.  SUDDENLY YOU WILL SEE, THE UNIVERSE IS MOVING AROUND YOU AND YOU ARE THE CENTER. LOOK FOR PEACE, YOU WILL ENJOY BLISS. DON'T LOOK FOR BLISS, YOU WILL ALWAYS LAND IN HOPELESSNESS. SECOND SUTRAYOUR MIND REFLECTS ON YOUR BRAIN AND YOUR BRAIN IS GIVEN A SPECIAL POWER TO REJUVENATE ITSELF IN ONE YEAR.  NOT ONLY THE AYURVEDA AND HINDU BIOLOGY TELLS THIS, BUT EVEN MODERN DAY SCIENCE AGREES THAT YOUR BRAIN COMPLETELY REPLACES ITSELF IN ONE YEAR. WHEN YOUR BRAIN REPLACES, REPLENISHES AND RECREATES ITSELF, IT CAN EITHER EXPAND ITS POSSIBILITY TO RADIATE PARAMASHIVA OR IT CAN SHRINK ITS POSSIBILITY TO RADIATE PARAMASHIVA. BOTH POSSIBILITIES EXIST BUT THERE IS NO NEUTRAL GEAR. THERE IS NO SUCH THING AS: ‘I AM STABLE’; EITHER YOU GO UP OR DOWN.  HAVE PRIDE THAT YOU HAVE PARAMASHIVA AS YOUR GURU. YOU HAVE PARAMASHIVA DIRECTLY TEACHING YOU AND INITIATING YOU. YOU DON'T EVEN NEED TO PRACTICE WHAT I AM TEACHING. IF YOU BELIEVE ANY OF THESE THREE STATEMENTS, OR ALL THESE THREE, THEN JUST STAND UP AND DO ATMA PRADAKSHINA, CIRCUMAMBULATION OF YOURSELF. CELEBRATE YOURSELF FOR BEING YOURSELF. YOU ARE WORTHY OF PRADAKSHINA NAMASKARA. IT IS A POWERFUL BLESSING:I THINK SWAMIJI LOVES ME.I KNOW FOR SURE SWAMIJI KNOWS THE ULTIMATE TRUTH.I THINK SWAMIJI TELLS THE ULTIMATE TRUTH TO ME. THIRD SUTRA I AM HAVING 25 HEADS, ONE CONSCIOUSNESS. ALL MY 25 HEADS ARE INTEGRATED INTO ONE CONSCIOUSNESS. THAT IS WHY I CAN THINK / MANIFEST 25 THINGS IN A COOL STRESS FREE WAY AT THE SAME TIME. IN YOU, YOU HAVE BROKEN YOURSELF INTO 25 CONSCIOUSNESS EVEN THOUGH YOU HAVE ONE HEAD. YOU GET PULLED AND PUSHED IN 25 DIRECTIONS.THAT IS WHY I AM SAYING: DENY THE EXISTENCE OF ALL SO-CALLED IDEAS OF SUFFERING, DELUSION OUTRIGHT. DON'T EVEN PUT THE LEG ON THE SLIPPERY ROCK. FOURTH SUTRAYOUR DECISION TO DENY THE EXISTENCE OF ANY FORM OF SUFFERING, ITS DELUSIONS, ITS ASPECTS, DIMENSIONS AND WHAT IS NOT MENTIONED HERE ALSO, MAKES SUCH A BEAUTIFUL SPACE IN YOU. YOU WILL SIMPLY START MANIFESTING AND PLAYING WITH THE POWERS. IT WILL GIVE YOU TREMENDOUS CONFIDENCE AND STRENGTHEN POWERFULNESS AND DENY THE EXISTENCE OF PAIN AND SUFFERING AND LOWER WAY OF EXISTING.FIFTH SUTRA: WHEN YOU START ACTIVELY PRACTISING THIS TRUTH, EXPRESSING IT IN YOUR INNER IMAGE WITH YOURSELF THROUGH YOUR OUTER IMAGE WITH OTHERS, ALL THE CONFLICTS WILL BECOME IRRELEVANT.TO WATCH THE FULL SATSANGH ON THE 5 TRUTHS (SUTRAS) AND RECEIVE THE INITIATION : HTTPS://WWW.YOUTUBE.COM/WATCH?V=8OY0MQHW6MK&FEATURE=EMB_TITLETO CHANT THE 5 TRUTHS (SUTRAS) - PLEASE VISIT HTTPS://SOUNDCLOUD.COM/NITHYANANDA-RADIO/FIVE-SUTRAS-BY-KAALABHAIRAVA_AUDIO-2021-01-21-AT-200937TO REGISTER FOR THE NEXT BHAVA SAMADHI DARSHAN ON THE 23RD FEBRUARY (TUESDAY) - VENKATESHWARA BHAVA SAMADHI DARSHAN PLEASE VISIT,See Translation104You, Ma Nithya KailaasaPriya, Sri Nithya Sadashivatmananda and 101 others15 Comments41 SharesLoveCommentShare

[washingtonmedicalgrouppc]

Washington clinical gathering - P. Steven Macedo - What is Rapid Eye Movement Habits Condition?

In REM rest conduct condition the individual presentations sporadic propensities with fast movement of the eyeballs while resting. It is similarly recognized as RBD, a rest parasomnia. It is a phase where an individual encountering this kind of Rapid Eye Movement issue gets outrageous, stunning and furthermore has savage dreams. The person truth be told begins acting as indicated by the thing he is dreaming. These activities can be of essential nature to complex developments. For instance, an individual can either move his feet in rest or maybe shout while fantasizing. This compromises for the individual that dozes close by the victim because of the furious exercises that are made by the patient while in a fantasy.

Washington clinical gathering

Quick Eye Movement activities issue is situated in individuals in the middle of the age of 15 and furthermore above, yet it is primarily a disease affecting matured people. This is fundamentally found in people that have a place with the age of 60 years. The medical condition is more normal in guys than in ladies. As indicated by an investigation, one-10th of the casualties are female and whatnot are male. Henceforth there are more incessant records of men harming their ladies allies while fantasizing than women harming their male accomplices.

Washington medical group

Consequences of the Disorder on a Person

Along these lines, you can comprehend the state of the individual dozing alongside the victim. This condition is risky for both the individual and furthermore their partner. During the REM rest, an individual's breathing winds up being unpredictable; they make fast eye-development rest, experience hypertension and furthermore there is loss of solid tissue atonia (loss of motion). In any case, all through the fantasies, the cerebrum is exceptionally vivacious and furthermore electrical errand of psyche recorded by EEG resembles when copied when the individual is conscious. Around 20-25 percent of rest time involves REM rest propensities issue.

Reason for this Disorder

The justification this condition in men as indicated by the examination study is because of the additional mileage of brainstem neurons existing to them. This condition sets up notwithstanding degenerative neurological conditions like Parkinson disease, multisystem decay, dissipated Lewy body dementia, just as Shy-Drager issue. Another reason is related with liquor withdrawal, tricyclic stimulant or serotonin reuptake counteraction use or different sorts of antidepressants.

P.Steven Macedo

Treatment of REM Problem

Treatment of this condition is conceivable through drug and furthermore lifestyle changes. The customary medication is the counter convulsant drug clonazepam. In spite of the fact that it is indistinct that precisely how it attempts to reestablish the muscle atonia, yet there is a worry whether it truth be told reestablishes the atonia or smothers bulk task.

Identifying with way of life changes, you can keep yourself at the protected side by putting sleeping pads on the deck or even a pad around the bed. This will get the individual and the individual dozing close by the individual from getting hurt if the customer leaves on the bed. Purchase a bed with upheld head board and furthermore place it away from mirrors just as home windows. You can likewise consider a bed with defended bedrails just as moreover wipe out some other risky things inside the space.

Forestalling liquor just as clinging to a rest routine moreover helps.est regimen additionally aids.

[kailaasainseremban]

WHAT IS BHAVA SAMADHI DARSHAN

परिकलित पुर्वौ कस् चमत्कर करि स्फुरति मम गरियन् एस मधुर्य पुरौ अयम् अहम् अपि हन्त प्रेक्स्य यम् लुब्ध चेतौ सरभसम् उपभोक्तुम् कमये रधिकेव ~ दर्पनद्ये देखि यदि अपन मधुरि; अस्वदिते लोभ होय् अस्वदिते नरि विचर कोरिये यदि अस्वद उपय; रधिक स्वरुप होइते तबे मोने धय

WHEN KRISHNA ONCE SAW HIS OWN EXTRAORDINARY SWEETNESS REFLECTED IN A JEWELLED WALL, HE WAS AMAZED AND SAID: “HOW UNPRECEDENTED AND ASTONISHING IS THIS DEEP AND INDESCRIBABLE SWEETNESS OF MINE! ALAS! WHEN I SEE IT, EVEN I BECOME GREEDY TO ENJOY ITS SWEETNESS, JUST LIKE RADHIKA! “WHEN I SEE MY OWN SWEETNESS IN THE MIRROR, I BECOME EAGER TO TASTE IT, BUT I CAN’T. AFTER DUE CONSIDERATION, I FIND THAT THE ONLY WAY TO RELISH THIS SWEETNESS IS THROUGH THE CONSTITUTION OF SRI RADHIKA.”

~ CHAITANYA CARITAMRTA ADI CH. 4

BHAVA SAMADHI DARSHAN IS A WINDOW TO THE INFINITE EXPANSE OF CONSCIOUSNESS, ALLOWING US TO GLIMPSE THE FORMLESS IN A WAY THAT WE CAN UNDERSTAND.

OUR VERY BIO-MEMORY AWAKENS TO THE SPACE OF PARAMASHIVA ULTIMATE CONSCIOUSNESS DURING BHAVA SAMADHI DARSHAN.

HAVING DARSHAN OR EVEN A GLIMPSE OF AN AVATAR CLEANSES THE KARMAS OF LIFETIMES, AND CREATES A DEEP AND LASTING TRANSFORMATION IN US.

DURING BHAVA SAMADHI DARSHAN, OUR NEURONS MIRROR THAT OF THE AVATAR.

MIRROR NEURONS ARE SPECIAL NEURONS THAT OBSERVE AND MIMIC THE ACTIONS OF THE AVATAR’S NEURON ACTIVITY INSIDE US JUST THROUGH SEEING. DURING BHAVA SAMADHI DARSHAN, OUR BEING COMES ALIVE AND CELEBRATES WITH THE ENERGY WAVE OF EXISTENCE. OUR VERY MUSCLES LEARN TO IMBIBE AND RADIATE PARAMASHIVA.

THE SCIENCE OF BHAVA SAMADHI DARSHAN KNOWS NO DISTANCE - A PHENOMENON MODERN SCIENCE IS JUST DISCOVERING AND TERMS AS QUANTUM TUNNELLING.

WHO IS KALABHAIRAVA?

MAHA KALABHAIRAVA IS THE LORD OF TIME AND SPACE. AS THE LORD OF TIME AND INTEGRITY, HE HOLDS THE KEY TO COSMIC ARCHIVES - THE AKASHIC RECORDS WHICH CONTAIN THE PAST, PRESENT AND FUTURE. KALABHAIRAVA IS THE SOURCE OF THE CAUSAL BODY, THE SOURCE FROM WHICH REJUVENATION FOR MANIFESTATION HAPPENS.

WHAT IS KAALA ?

KALA IS THE DIMENSION OF THE UNIVERSE IN WHICH THE VIBRATION COMPONENT, THE PARASHAKTI COMPONENT OF PARAMASHIVA IS MANIFESTING.

JUST ZOOM OUT, SEE THE SPACE WHERE BIG BANGS AND BLACK HOLES ARE HAPPENING SIMULTANEOUSLY, BILLIONS OF PLANETS, SUNS, MOONS, STARS MOVING, TAKING BIRTH, LIVING FOR MILLIONS OF YEARS AND DISAPPEARING SIMULTANEOUSLY. THAT SPACE IS KAALA.

THE KAMIKAGAMA, PURVA PADA, MANTRODDHARA PATALAM, VERSE - 24 SAYS

SWASTHAM THIKSHNA SHOBITHAKARAM SHRUTHAJANOTH DHAARAM KRUPASAGARAM

AAMNAYASKAROTHI KARPAKARAM DANDAM DARATNAM SADA

SHRI KAASIPURANAYAKAM SAKALA MANTRASYA ISHWARAM MOKSHADAM

DHYAYETTAM HRIDHI KALABHAIRAVA GURUM KAANTHA SAMETAM PARAM.

FURTHER, THE SKANDA PURANA SAYS

AT ONE POINT, BRAHMA THE CREATOR, FALLS INTO DELUSION AND FORGETS HIS REAL IDENTITY. HE ORIGINALLY HAD 5 HEADS, JUST LIKE MAHADEVA. SUDDENLY HE FELL INTO DELUSION, CATCHING ON TO HIS FALSE IDENTIFY DUE TO HIS EGO AND ARROGANCE. SO, MAHADEVA JUST WAKES UP FROM HIS SAMADHI, MANIFESTS AS KALABHAIRAVA, THE LORD OF TIME, REMOVES THE FALSE IDENTITY OF BRAHMA AND BLESSES HIM WITH THE SHIVOHAM EXPERIENCE.

LORD KALABHAIRAVA BESTOWS ABUNDANCE AND WEALTH

भुक्तिमुक्तिदायकं प्रशस्तचारुविग्रहं

भक्तवत्सलं स्थितं समस्तलोकविग्रहम्

BHUKTI-MUKTI-DAAYAKAM PRASHASTA-CAARU-VIGRAHAM

BHAKTA-VATSALAM STHITAM SAMASTA-LOKA-VIGRAHAM

KALABHAIRAVA ASHTAKAM - VERSE 4

(SALUTATIONS TO SRI KALABHAIRAVA) WHO IS THE GIVER OF WORLDLY PROSPERITY AND LIBERATION AND WHO HAS AN AUSPICIOUS PLEASING FORM. WHO IS KIND AND LOVING TO HIS DEVOTEES AND WHO STANDS FIRM AS THE DEITY OF ALL THE LOKAS.

WHAT IS KALABHAIRAVOHAM

THE SUPREME PONTIFF OF HINDUISM, JAGATGURU MAHASANNIDHANAM, HIS DIVINE HOLINESS BHAGAVAN NITHYANANDA PARAMASHIVAM BLESSED HUMANITY WITH MAKING THE INITIATION INTO THE 5 TRUTHS (SUTRAS) TO MANIFEST MAHAKALABHAIRAVA REVEALED ON THE 17TH OF JANUARY 2021, AS AN EXPERIENCE WITH THE KALABHAIRAVOHAM PROGRAM.

THE 5 TRUTHS (SUTRAS) ARE:

FIRST SUTRA

SUTRA 1 - THE PERSON, BEING, WHO IS BOLD ENOUGH TO DENY THE EXISTENCE OF SUFFERING AND PAIN IN YOUR LIFE EVEN IF YOUR MIND BRAINWASHES YOU AND FORCES YOU TO BELIEVE THAT SUFFERING EXISTS, IN FRONT OF THAT MIND, IF YOU BOLDLY STAND AND TERRORISE THAT MIND BY YOUR POWERFUL WAY OF DENYING THE EXISTENCE OF SUFFERING, YOU BECOME THE SPACE OF MAHA KALABHAIRAVA AND NO KARMA TOUCHES YOU AND YOU ESTABLISH YOURSELF IN THE NEUTRAL ZONE CALLED NIRVIKALPA SAMADHI.

JUST DENY TO ACCEPT THE EXISTENCE OF PAIN AND SUFFERING. DO NOT LOOK FOR SOLUTION, FOR COMPROMISED UNDERSTANDING, QUICK RELIEF OR ALTERNATIVE METHODS.

FOR ALL MY DISCIPLES FOR WHOM I AM TRUTH, TRUTH, TRUTH, NOTHING BUT TRUTH, SATYA, I AM GIVING YOU THIS INITIATION. YOU WILL ALL BE SUCCESSFUL IN THIS INITIATION AND TRUTH.

WHEN YOU DENY OUTRIGHT THE EXISTENCE OF PAIN AND SUFFERING, THE WHOLE CHANGE HAPPENS IN YOUR SYSTEM, CREATES SPACE FOR PARAMASHIVA. SUDDENLY YOU WILL SEE, THE UNIVERSE IS MOVING AROUND YOU AND YOU ARE THE CENTER. LOOK FOR PEACE, YOU WILL ENJOY BLISS. DON'T LOOK FOR BLISS, YOU WILL ALWAYS LAND IN HOPELESSNESS.

SECOND SUTRA

YOUR MIND REFLECTS ON YOUR BRAIN AND YOUR BRAIN IS GIVEN A SPECIAL POWER TO REJUVENATE ITSELF IN ONE YEAR. NOT ONLY THE AYURVEDA AND HINDU BIOLOGY TELLS THIS, BUT EVEN MODERN DAY SCIENCE AGREES THAT YOUR BRAIN COMPLETELY REPLACES ITSELF IN ONE YEAR. WHEN YOUR BRAIN REPLACES, REPLENISHES AND RECREATES ITSELF, IT CAN EITHER EXPAND ITS POSSIBILITY TO RADIATE PARAMASHIVA OR IT CAN SHRINK ITS POSSIBILITY TO RADIATE PARAMASHIVA. BOTH POSSIBILITIES EXIST BUT THERE IS NO NEUTRAL GEAR. THERE IS NO SUCH THING AS: ‘I AM STABLE’; EITHER YOU GO UP OR DOWN. HAVE PRIDE THAT YOU HAVE PARAMASHIVA AS YOUR GURU. YOU HAVE PARAMASHIVA DIRECTLY TEACHING YOU AND INITIATING YOU. YOU DON'T EVEN NEED TO PRACTICE WHAT I AM TEACHING.

IF YOU BELIEVE ANY OF THESE THREE STATEMENTS, OR ALL THESE THREE, THEN JUST STAND UP AND DO ATMA PRADAKSHINA, CIRCUMAMBULATION OF YOURSELF. CELEBRATE YOURSELF FOR BEING YOURSELF. YOU ARE WORTHY OF PRADAKSHINA NAMASKARA. IT IS A POWERFUL BLESSING:

I THINK SWAMIJI LOVES ME.

I KNOW FOR SURE SWAMIJI KNOWS THE ULTIMATE TRUTH.

I THINK SWAMIJI TELLS THE ULTIMATE TRUTH TO ME.

THIRD SUTRA

I AM HAVING 25 HEADS, ONE CONSCIOUSNESS. ALL MY 25 HEADS ARE INTEGRATED INTO ONE CONSCIOUSNESS. THAT IS WHY I CAN THINK / MANIFEST 25 THINGS IN A COOL STRESS FREE WAY AT THE SAME TIME. IN YOU, YOU HAVE BROKEN YOURSELF INTO 25 CONSCIOUSNESS EVEN THOUGH YOU HAVE ONE HEAD. YOU GET PULLED AND PUSHED IN 25 DIRECTIONS.THAT IS WHY I AM SAYING: DENY THE EXISTENCE OF ALL SO-CALLED IDEAS OF SUFFERING, DELUSION OUTRIGHT. DON'T EVEN PUT THE LEG ON THE SLIPPERY ROCK.

FOURTH SUTRA

YOUR DECISION TO DENY THE EXISTENCE OF ANY FORM OF SUFFERING, ITS DELUSIONS, ITS ASPECTS, DIMENSIONS AND WHAT IS NOT MENTIONED HERE ALSO, MAKES SUCH A BEAUTIFUL SPACE IN YOU. YOU WILL SIMPLY START MANIFESTING AND PLAYING WITH THE POWERS. IT WILL GIVE YOU TREMENDOUS CONFIDENCE AND STRENGTHEN POWERFULNESS AND DENY THE EXISTENCE OF PAIN AND SUFFERING AND LOWER WAY OF EXISTING.

FIFTH SUTRA:

WHEN YOU START ACTIVELY PRACTISING THIS TRUTH, EXPRESSING IT IN YOUR INNER IMAGE WITH YOURSELF THROUGH YOUR OUTER IMAGE WITH OTHERS, ALL THE CONFLICTS WILL BECOME IRRELEVANT.

TO WATCH THE FULL SATSANGH ON THE 5 TRUTHS (SUTRAS) AND RECEIVE THE INITIATION : HTTPS://WWW.YOUTUBE.COM/WATCH?V=8OY0MQHW6MK&FEATURE=EMB_TITLE

TO CHANT THE 5 TRUTHS (SUTRAS) - PLEASE VISIT HTTPS://SOUNDCLOUD.COM/NITHYANANDA-RADIO/FIVE-SUTRAS-BY-KAALABHAIRAVA_AUDIO-2021-01-21-AT-200937

[juniperpublishers-oajnn-blog]

Individual Neuronal Apoptosis Provokes DeterminedNecrosis of the Regional Cerebral Infarct in Patients with Ischemic Stroke

Authored by  Lawrence M Agius

Abstract

Interplay pathway dynamics are constitutive agonists in an evolving ischemic focus within the brain that is triggered by apoptotic programmed cell death that is subsequently established as a necrotic focus of infarction within the cerebral cortex of many patients with stroke. The evolutionary dynamics further permit the activation of potentially neuroprotective measures that primarily attempt limitation of involvement of adjacent less injured neurons but subsequently by the establishment of transformed penumbra to a necrotic focus of infarction. Within such contextual transformations, the individual apoptotic neuron determines the characterized infarcted region as necrotic focus formulation. Individual neuronal apoptosis provokes determined necrosis of the regional cerebral infarct in patients with ischemic stroke.

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Introduction

Stroke patients comprise a large number of patients with a highly significant degree of cerebral ischemia that is best exemplified by the transient focal ischemia models in experimental animals such as rat and mouse. Mechanisms include bioenergetic failure and loss of cell homeostasis, and also acidosis, excitotoxicity and disrupted blood-brain barrier [1]. A central issue is the series of set conditioning factors that induce apoptosis of individual neurons within the penumbral region of the cerebral cortex on the one hand and the development if neuronal necrosis on the other. Combined steroid administration inhibits ischemia-induced apoptosis of neutrons through involvement of the intrinsic pathways [2]. It would appear that a combination of both apoptosis and necrosis of neurons evolves in at least some of the patients, and indeed neurons may exhibit features of both these forms of neuronal cell death when electron microscopic studies are combined with molecular and biochemical modes of analysis. Whether necrosis or apoptosis occurs often depends on cell type, cell age and location in the brain. Apoptosis leader to protein crosslinking, DNA fragmentation, ligand expression for phagocytic cell receptors and subsequent phagocytic uptake [3].

Neuroprotection

It is idealized that a set of potentially neuroprotective mechanisms is activated within the penumbral region of an evolving cerebral infarct. Oxidative stress contributes to ischemia/reperfusion with blood-brain barrier disruption, inflammation necrosis and apoptosis; Nnclear factor-E2-related factor 2 is central to regulated antioxidant defence and may protect against ischemia-induced neuronal injury [4]. Such coupled phenomena are central to the establishment of the expanding infarct secondary to delayed death of more neurons in the few days following the primary acute infarction of the core lesion. Glycine inhibits tumor necrosis factor alpha and protects agains inflammation and gloss in hypoxia-ischemia of neurons [5]. Such considerations are believed to potentiate the possible beneficial attempts at reducing infarct size within the acute dimensions of ischemic injury to neurons.

Glial cells

Glial cells such as astrocytes and microglia are implicated in neuroprotection and indeed the cellular network of gap junctions between individual astrocytes are viewed as supportive elements in neuroprotection. The dimensions of complex control of ion-motive ATPase channels collaborate with the dynamics of possible recovery of related ischemic neurons that implicate a regional characterization and re-characterization of the ischemic injury not only to individual neurons but also to groups and sizeable aggregates of such neurons. Auto-antibodies to apolipoprotein A-1 are associated with poorer clinical recovery and increased brain lesion volume 3months after acute ischemic stroke [6].

Dynamics of ischemic injury

Genetic evidence exists that separates apoptosis from necrosis through different forms of nuclear pyknosis, with conservation of nuclear pyknosis in the propagation of necrosis [7]. Performance dynamics of the acute ischemic focus also implicates microglia that are implicated in removal of ischemic individual neurons following acute ischemic injury. The distributional coherence of integral groups of ischemic neurons is hence mirrored by presumably apoptotic individual neurons undergoing damage primarily to mitochondria and to lipid moieties of the plasma membrane of the cells. In such context, the evolving participation of apoptosis and necrosis would permit the progression of caspase pathway activation and the release of cytochrome c release from mitochondria. Also, destabilized cellular calcium homeostasis follows a stereotyped pattern of changes that invokes execution pathways of neuronal cell injury.

The phagocytic receptor CED-1 is activated through interaction with its ligand phosphatidylserine (PS) exposed on the surface of necrotic neutrons; calcium influx activates a neuronal PS-scramblase for PS exposure [8]. A complex array of executing agonists include excitotoxic, oxidative and lipid peroxidation, and metabolic insults such as hypoglycemia participates within contexts of activated apoptotic pathways, as evidenced by the neuroprotective effects of administered caspase inhibitors in the acute phase of ischemic insults. Epigenetic regulatory networks in ischemic stroke may protect against oxidative stress with induced DNA methylation, histone modification and microRNAs, with affected redox state in neutrons, glia and vascular endothelial cells [9].

Determined pathway events

Determined outcome of the ischemic individual neuron and also of groups of such neurons is affected by "ischemic preconditioning" whereby a mild episode of ischemia generates resistance to a second ischemic episode. Certainly, the panoramic contexts of evolving ischemic injury within neurons is programmed within the pathways primarily dictated by individual cellular responses to ischemia that however originates as a regional focus of groups of ischemic neurons. Platelet- activating factor receptor is expressed on cellular and nuclear membranes of leukocytes, platelets, endothelial cells, neurons and microglia; its deficiency is experimentally associated with prevention of caspase-3 activation and decreased vascular permeability and cerebral edema. Decreased brain levels of tumor necrosis factor-alpha, interleukin-1beta and the chemokine (C-X-C motif) ligand 1 may be crucial in global brain ischemia-reperfusion [10].

Particularly intriguing is the overlap of regional and individual cell ischemic episodes that determine the onset of a core of necrotic cerebral tissue in the first instance and the subsequent creation of a penumbra of regional and partially injured neurons and glial cells. It is further to such phenomena that the ischemic episodes are regional also as evidenced by activated neuroprotective mechanisms such as the action of neurotrophic factors and of some cytokines such as tumor necrosis factor alpha and interleukin 1-beta. The PPAR gamma agonist 15d-PGJ2 regulates microglial activation and decreases tumor necrosis factor aha and interleukin-1 expression. Fewer apoptotic cells and less CD68 positive staining in diabetic schema rats [11].

Chaperone dysfunctionality allows for an evolving train of events in the execution of both apoptosis and necrosis within the individually affected neurons and as further portrayed by the dynamics of the expanding penumbral region. 4'-O-beta- D-Glucosyl-5-O-Methylvisamminol, a natural histone H3 phosphorylation epigenetic suppressor is a neuroprotective factor by acting via the PI3K/Akt singling pathway in focal ischemia in rats [12]. It is further to such processes that the integral identity of cell-death phenomena permits the execution of individual cell damage as dictated by regional injuries to the cerebral cortex in particular. pH gradient difference around cerebral foci of ischemia may allow delivery of polyethylene glycol-conjugated urokinase nano gels with effective thrombolysis of the ischemic stroke [13].

Performance attributes

Performance attributes characterize hence the emergence of a necrotic core to the ischemic focus in a manner that potentiates the evolutional progression of the penumbral region of partially injured neurons. MicroRNA-9 is down regulated in mice with middle cerebral artery occlusion and oxygen-glucose deprivation neurons, with suppression of neuronal apoptosis on its up regulation [14]. The parameters of acquisition of cellular ischemic injury is mirrored in the evolutionary course dynamics of such events as the emergence of a multitude of agonists that portray the character of primary core necrosis by the penumbral region of conditioned delay of individual cell death within contexts of transforming apoptotic cascades within such individual neurons.

Apoptosis

The ischemic neuron undergoing apoptosis is generally associated with adjacent cells that do not show apoptosis phenotype characteristics and as such this has implicated microglial phagocytosis of the individually damaged neuron. Such a phenomenon however is contrary to the widespread focus of integral ischemic injury to the cerebral cortical region and is also at variance with a presumably programmed response to injury to cellular networks. Tissue necrosis in particular is a conceptual realization of regional fields of perfusion and re-perfusion events arising from compromised individual vessels of supply. Penehyclidine hydrochloride down regulates the phosphorylation of JNK, p38MAPK, and c-Jun and protects neutrons against ischemia/reperfusion [15]. Ongoing phenomena such as the no-reflow events within the vessels of supply allow for complicated series of processes involving neuroprotective measures. Scite;;arom down- regulates expression of angiotensin-converting enzyme and ATI receptor with neuroprotective effects [16]. The activation of heat shock protein such as HSP-70 and increased secretion of glucocorticoids during the acute ischemic episode allows for the emergence of constitutive pathways that on the one hand further injure the neurons and on the other hand actually enhance potential resistance to acute neuronal ischemia.

Apoptosis/necrosis interplay

The apoptotic neurons exhibit characteristic cell body shrinkage and condensation of chromatin that progresses as fragmentation of the DNA and the appearance of single- and double-strand breaks of the DNA molecules. Such events may be related to the cytoskeletal injuries that occur in individual neurons such as those caused by depolymerization of actin filaments by gelsolin. Release of calcium from endoplasmic reticulum stores is characterized as an end-pathway that is reflected in individual cell death. Mitochondrial dysfunction further correlates with the onset and participation of injurious events as evidenced by programmed cell death pathway activations. Apoptosis of individual ischemic neurons is hence a contextual setting for necrosis of core foci within the lesion as further indicated by the subsequent establishment of a truly necrotic focus of cerebral infarction. The delivery of multi-components would further confirm the derivation of programmed cell death as determining agonist series of pathway events in establishment of further increased injury to individual neurons and regional groups of ischemic neurons. Etanercept, a recombinant TNF receptor (p75)-Fc fusion protein, may with repeated administration prevent exacerbation of cerebral ischemic injury in the diabetic state, mainly through anti-inflammatory action [17].

Go to

Conclusion

Dynamics of calcium influx and of calcium release intracellularly include the participation of neuronal programming in cell death that is regionally characterized by dynamics of individual neuronal self-programmed cell death. As is evidenced by such dynamics of processed de-control of agonists such as mitochondrial dysfunction with release of cytochrome c and the lipid peroxidation pathways on the one hand, and of the oxidative end-products primarily affecting membrane lipids and calcium membrane channels, on the other, there evolves a regional/individual cell interplay of integral ischemic and hypoxic elements in the pathogenesis of cerebral infarcts. In such terms, evolutionary dynamics is collaborated pathway event in re-characterized potential neuroprotection of adjacent neurons within the adjacent cerebral cortex in many patients suffering from ischemic stroke. On the other hand, the transforming dimensions of injury to neurons are interplay supportive elements that profile-determine cell apoptosis that, in turn, may lead to potential necrosis of cerebral tissue.

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Open Access Journal of Neurology & Neurosurgery in Full text in Juniper Publishers

https://juniperpublishers.com/oajnn/OAJNN.MS.ID.555612.php

[creativesage]

(via A step-by-step guide on how to choose, make, and keep New Year’s resolutions – Harvard Gazette)

Moving forward, even slowly, puts your goals within reach.

A 12-step guide to keeping those resolutions

As the holiday music fades and the time to pay the resolutions piper comes due, let Harvard experts make the transition a little easier. Don’t know where to start? You can try the 1 percent performance improvement method. Stressed at the prospect of a lifestyle change? Practice mindfulness and find out how meditation can lead to a “better brain” in just eight weeks. Want to extend that? Learn what 80 years of Harvard research has to say about living a longer and happier life.

Still not sure what will suit you best? Pick a topic from the Harvard T.H. Chan School of Public Health’s Nutrition Source, where you’ll find advice that goes far beyond your plate and that first cup of coffee in the morning.

The key is to choose your New Year’s resolution, and make it happen. MacKenzie Kassab, a former contributor to the Division of Continuing Education’s Professional Development website, put together a 12-month plan for making — and keeping — resolutions filled with the advice of experts from Harvard and beyond.

Let’s take a look.

January: Ready, set, goal

This is it: the time to think ahead about where — and who — you want to be this year.

“I don’t think there’s such a thing as a goal too big,” says Margaret Andrews, president of Mind and Hand Associates consulting firm and an instructor for the Harvard Division of Continuing Education.

So reach for the stars! But remember, even astronauts have to contend with bad weather. “You have to think about your ecosystem,” Andrews says. What external factors could prevent you from reaching your goal?

You might resolve to eat healthy foods and lose five pounds around your midsection. That’s reasonable enough. But how will you cope with those 3 o’clock sugar cravings? What will you do when your oblivious spouse stocks the cabinet with cookies and chips? Is there something beyond your control that could be a barrier to success? Keep it in mind, but don’t get discouraged.

“Consider what you need to start doing or stop doing, and anticipate obstacles,” Andrews says. “If you don’t think about it now, then you’ll have no willpower in that moment.” Have a strategy in place, and you’ll be on your way to reaching that goal in no time.

February: Commit to a process

You’ve set your sights on a goal. Now, devise a plan.

Entrepreneur and author of “Atomic Habits” James Clear recently told Inc. magazine that simply setting a goal is the first step on the road to unhappiness.

“You’re essentially saying, ‘I’m not good enough yet, but I will be when I reach my goal.’ The problem with this mindset is that you’re teaching yourself to always put off happiness and success until the next milestone is achieved,” Clear says.

Instead, he suggests focusing on a process, not the end result. Deconstruct your goal into productive, workable actions.

Finding a new job is a common resolution. But the hunt can be daunting. To make it more manageable, establish a schedule: send out two résumés a week, or attend one networking event a month.

By celebrating small victories, the journey becomes as meaningful as the destination.

March: Find your motivation

“There’s no one-size-fits-all solution when it comes to motivation,” Andrews says. “Some people go whole hog, and others ease themselves in. You really have to know yourself and what works for you.”

This is the time to explore what lights your fire. If your goal is to run a marathon, you might find the most encouragement in rewarding small wins. Reach 10 miles, book yourself a massage.

If that doesn’t work for you, see if a picture of Usain Bolt on the refrigerator is enough to keep you moving. Explore tactics until you find one that fits, and don’t be afraid to get creative.

April: Shout your intentions

If your ambition is waning, proclaim your intentions from the rooftops. Text friends, email close colleagues, or call your mom.

“When we advertise our desire to change, we are openly risking failure, putting our reputation and self-respect on the line,” says Marshall Goldsmith, executive coach and author of “Triggers.” “It’s the difference between betting on ourselves with hard-earned cash and settling for a friendly no-money wager.”

Encouragement is a positive byproduct — most people will want to see you succeed, and some may even offer support or guidance.

A Harvard study, almost 80 years old, has proved that embracing community helps us live longer, and be happier.

May: Question everything you’re doing

One of Goldsmith’s “magic moves” for changing behavior is daily self-questioning. He suggests composing a list of queries that encourage reflection.

Someone aiming to gain three new clients this year might ask, “Did I do my best to generate leads today?” Meanwhile, someone who wants a heftier savings account could inquire, “Did I do my best to avoid unnecessary spending today?”

There are no rules, other than tracking progress with the same questions each day, and just one suggestion: starting each question with “Did I do my best to …”

“This phrase injects personal ownership and responsibility into the Q&A process,” he says.

June: Reassess your goals

You’re halfway through the year, and your goal is in sight! Or perhaps not. If things aren’t going as planned, reconsider your strategy and be honest about what your resolution is worth to you.

“Someone I know was trying to lose weight, and she was told she’d need to cut out her nightly glass of wine,” Andrews says. “She knew herself well enough to say, ‘That’s a pleasant part of my life, and I’m not willing to give it up.’ She found other ways to compensate.” Look at which tactics have been less effective to this point, and explore other ways of reaching your goal. Maybe you add 15 minutes to your workout but keep the pinot noir.

Tweaking your expectations might also be acceptable. “You may want to be the weight you were at 18, but are you really willing to do everything required to get there?” asks Andrews. Fitting into a snug pair of jeans from last year might be a reasonable compromise, especially once you’ve seen what success demands.

July: Find support

There’s a reason support groups exist for everything from addiction to breastfeeding: There’s power in numbers. Social support can be instrumental to accomplishing goals.

“Hang with the right crowd and their success can inspire us to think, ‘If they can do it, I can too!’” says Piers Steel, the researcher behind “The Procrastination Equation.”

Find an organization whose mission aligns with yours, whether it’s Weight Watchers, Habitat for Humanity, or the Society of Women Engineers. A gap in the market is a great excuse to create your own goal-oriented group, which might be just a handful of colleagues sharing professional growth strategies over dinner. “Giving up or continuing to strive — both are contagious,” Steel says.

August: Get energized

All goals, personal or professional, require adequate energy. Unfortunately, things like stress, caffeine, alcohol, and late nights can sap stamina. Willpower and motivation are often the next to go.

A lifestyle overhaul is extreme, but minor changes add up. First, purge your living or workspace of distractions, whether that means clearing clutter from your desk or uninstalling the Facebook app from your phone. Steel advises “strategically allocating” limited energy reserves. Less mess, literal or figurative, equals more mental focus.

Next, determine when you’re most efficient, and dedicate part of that time to meeting your goal. Are you a morning person striving to become fluent in French? Put on Radio France Internationale while getting ready for work. Is your head clearest in the afternoon? Pull out les leçons on your lunch break.

And don’t neglect your mental and physical health. “Your energy stores are a limited resource, so actively replenish them,” Steel says. That means nurturing your well-being — and getting a good night’s sleep.

September: See results

Close your eyes. Now, imagine meeting your goal. Are you holding a gold medal? A bigger paycheck? A jaw-dropping baked Alaska? According to Steel, “The detailed mental re-creation of a performance engages mirror neurons that engrave the act in your brain almost as deeply as if you were actually practicing it.”

The next — and most important — step is called mental contrasting: visualizing where you are today, with an empty trophy case, bank account, or oven. “The result will be that your present situation becomes framed as an obstacle standing in the way of your dreams,” says Steel.

Contrasting where you are and where you want to be sparks exactly the motivation most people need to spring into action.

October: Get inspired

Bill Gates reads a reported 50 books a year. In fact, the Microsoft co-founder is so passionate about reading that he started the GatesNotes blog to post reviews of his favorite titles. “Shoe Dog,” by Nike’s Phil Knight, is at the top of the list. “Knight opens up in a way few CEOs are willing to do,” writes Gates. “He tells his story as honestly as he can. It’s an amazing tale.” And an inspiring one, even for one of the world’s most powerful men.

Books and movies can provide the encouragement we can’t always get from people around us. “Rocky” gives hope to the underdog. “The Pursuit of Happyness” suggests that anything’s possible. Search for plots that strike a chord. “The most effective [biographies] will resonate with your own background,” Steel says.

Not everyone can plow through a book a week, but motivational speeches and podcasts stream from all corners of the internet. “Great athletes, heroes, and entrepreneurs regularly speak about their experiences,” says Steel. “Seek them out.”

Get inspired on your morning commute, and you’ll be surprised what you can accomplish throughout the day.

November: Ask for help

Another of Goldsmith’s magic moves is asking for help. “Few people will refuse your sincere plea,” he says. “Asking for help sustains the change process, keeps it moving forward.”

When you hit a stumbling block, call on friends who’ve accomplished similar goals or on your professional mentor. Most people will be honored you came to them for support.

And when you’re ready to wave the white flag, call in the experts. There are resources to support just about every ambition, from amateur cooking classes to professional development programs. Even Beyoncé worked with a vocal coach to reach her goal of world domination.

December: Applaud success — or lessons learned

The end of the year is a time to reflect on progress toward your goal or to pat yourself on the back for achieving it.

Is there any shame in not fulfilling a resolution? “It depends on the goal,” says Andrews. “If it’s to stop doing something abusive to yourself or someone else, it’s probably not a good one to give up on. Or it might turn out your goal wasn’t really what you were going after. You know what? It’s your life, and you get to decide that. Failure isn’t failure if you learn something from it. It’s just a way station on the way to success.”

Contemplate this year’s obstacles and processes, and rework your strategy for next year. There’s rarely a deadline for prosperity.

Ready to start?

Develop your personal plan for meeting your resolutions with a 12-month worksheet you can download here.

[Entire post — click on the title link to read it at the Harvard Gazette.]

***

You’re working on your goals, and your team’s goals. We can help you spring into action and develop a real plan that you can implement in a smart way, so you’ll start seeing results immediately, before you feel discouraged. If you feel that you’ve already gone off-track, we can help you get your focus, courage, and motivation back.

At  Creative Sage™, we often coach and mentor individual clients, as well as work teams, in the areas of change management, building resilience, making personal, career or organizational transitions — including to retirement, or an “encore career” — and facilitating development of leadership, creativity and collaboration capabilities. We also work with clients on work/life balance, finding purpose and meaning, focus and productivity issues, and how to present themselves and their ideas more effectively in professional situations.

We guide and mentor executives, entrepreneurs, intrapreneurs, artists, and creative professionals of all generations, to help them more effectively implement transition processes, and to become more resilient in adjusting to rapid changes in the workplace — including learning effective coping techniques for handling failure, as well as success. We work with on-site and virtual teams.

Please do not hesitate to contact us if you would like to discuss your situation. You can also call us at 1-510-845-5510 in San Francisco / Silicon Valley. Let’s talk! An initial exploratory phone conversation is free. When you talk with me, I promise that I’ll always LISTEN to you with open ears, mind and heart, to help you clarify your own unique path to a higher vista of success.

              ~Cathryn Hrudicka, Founder, CEO and Chief Imagination Officer of Creative Sage™, Executive Coach, Consultant, and Mentor.

***

[sabertoothriena]

Your Culture X My Culture: A Guide To Being Nice

‘Culture’ is a big word. Since it’s Gemini season (Moon in Gemini here, hola!), I’m going to try and unpack how I navigated through a 3-year-long ‘cultural exchange’ through my experience with language at university.

When I first started my lessons at Royal Holloway, I remember how certain white British people would turn their noses up at me simply because I communicated differently. Only a rare handful put in the effort to understand where I was coming from. By ‘different’ I mean that I had to catch myself whenever I slurred or cut my words short in order to compress them into a sound that fit the accent they were already used to. Basically, I was begging my mirror neurons to work for me every time I had to attend a class all throughout my first year. Trying on the one hand was difficult. Feeling like my communicated message wasn’t accepted was a whole other ballgame. Was it that deep? Yes, it was, and is still that deep.

I can break my interactions with people whom I am considered ‘foreign’ to down into three tiers, and each tier requires a bit of a leap to reach the other, in this order:

1 - You make an effort to understand what I am saying.

2 - You understand what I am saying, and ACCEPT what I am saying.

3 - You ask and LEARN how to speak like me in order to get a glimpse of my experience and process whenever I code-switch to sound like you. (This requires learning on your part to even begin considering snippets of my history and culture that I carry with me wherever I go, and to communicate with me on that level while acknowledging that you don’t know and will never know everything about the place I come from as you converse with me. And I will do the same with you.)

I still speak in a different accent when I communicate with my British friends and can code-switch back to Singlish whenever I want, but a question I’ve been asking myself is this: ‘Why do I feel the need to speak in an accent in the first place?’ It’s a pressure-cooker of a question, but it is important to me that I am able to answer it. I am confronting that question today.

Did I trust that the Brits could understand my Singaporean accent? No. And by the way, I am impatient as hell, so I learned to speak the way they did in order to communicate messages across in an efficient, surefire way. Did I compromise on my own cultural identity especially since language is such a big part of it? Yes, actually. But I don’t regret it because I saw myself as a guest in their country, though I believe it is their privilege to learn how to speak like me.

I definitely attach pride to my ability to code-switch. Dear reader, you may find the next statement a contentious one, but here goes: I find myself being able to articulate my ideas more when I speak in a British accent. There are certain idiosyncratic words and phrases that express a whole range of various meanings compared to the English/Singlish vocabulary I am already exposed to. There is a certain confident or poise I perform whenever I speak in an accent, and I like how my mind works when my mouth runs on accented, Brit-English fuel.

This is very personal by the way, and I am by no means saying that people are unable to express themselves while speaking Singlish/Singaporean English as compared to the British accent. It just means that I like how I am able to express myself in a different way. Up till today, it is as if speaking in a British accent unleashes a whole other world of speech and expression in my being. There is a different vibe, and with that different vibe comes a new meaning of what it means to even coming close to calling Britain a ‘home’. When I was at university, I would also delight in the fact that I could speak Singlish among my friends and feel connected to both worlds. Strange, yet familiar.

One night, I found myself hanging out with two male friends, the first being a black British, Jamaican-born man and the other a British Lebanese (and ultimate Drake-wannabe, lol) under a shelter in complete darkness except for the red glow of the cigarette we shared. I looked at them and said, “Guys, our backgrounds are so different, yet here we are.” And we simply nodded and grinned in agreement. This is a picture of what Tier 3 (as above) looks like. Another Tier 3 incident was when Tammy started singing a string of Hokkien expletives I had taught her in class. It just so happened that a Malaysian playwright had come in to teach us that day. He smiled and looked at her before turning to me, asking, “So where are you from?” “Singapore.” “Ah.” That was classic.

What’s my point? I learned more by speaking their way, and I relished it.

But never once did I hesitate to correct my friends’ intonations when they used ‘lah’ or ‘leh’ wrongly. You should’ve seen the look on my face when the Dean of the English department pronounced my name wrongly at graduation and added another syllable from god knows where. I was livid.

This is how we communicate and practice acceptance. It’s not very difficult, but it’s definitely not as simple, either.

By the way, to all you culture vultures reading this: three months is definitely way too short for a cultural exchange. If you’re plannning on going for one, make it a worthwhile one. Go for a year if you can afford it. Take your time at each destination if you’re going backpacking. Don’t just make a friend - learn HOW to make a friend. Sure, your mirror neurons will probably be on fire every single day while you’re in a foreign country, but that’s the fun of it, innit.

[drangsaldrangsal]

Effects of Obesity Can Mirror Those of Aging

In a new paper, published in the journal Obesity Reviews, researchers from Concordia University in Montreal, Quebec, argue that obesity should be considered premature aging.

The study looked at how obesity predisposes people to developing several life-altering or life-threatening diseases typically seen in aging individuals: compromised genomes, weakened immune systems, decreased cognition, increased chances of developing type 2 diabetes, Alzheimer’s disease, cardiovascular disease, cancer and other illnesses.

The research team reviewed more than 200 papers that analyzed obesity’s effects, from the level of the cell to tissue to the entire body.

“We are trying to comprehensively make the argument that obesity parallels aging,” said Dr. Sylvia Santosa, associate professor of health, kinesiology and applied physiology in the Faculty of Arts and Science, and a Tier II Canada Research Chair in Clinical Nutrition.

“Indeed, the mechanisms by which the comorbidities of obesity and aging develop are very similar.”

The study was co-authored by Drs. Bjorn Tam, Horizon postdoctoral fellow, and José Morais, an associate professor in the Department of Medicine at McGill University.

The paper looks at ways obesity ages the body from several different perspectives. Previous research has already linked obesity to premature death. But the researchers note that at the lowest levels inside the human body, obesity is a factor that directly accelerates the mechanisms of aging.

For example, the team looked at the processes of cell death and the maintenance of healthy cells — apoptosis and autophagy, respectively — that are usually associated with aging.

Studies have shown that obesity-induced apoptosis has been seen in mice hearts, livers, kidneys, neurons, inner ears and retinas. Obesity also inhibits autophagy, which can lead to cancer, cardiovascular disease, type 2 diabetes and Alzheimer’s.

The researchers also write that obesity influences a number of gene alterations associated with aging. These include the shortening of telomeres, the protective caps found on the ends of chromosomes. Telomeres in patients with obesity can be more than 25 percent shorter than those seen in control patients, for example.

The authors further point out that obesity’s effects on cognitive decline, mobility, hypertension and stress are all similar to those of aging.

In addition, obesity plays a significant role in the body’s fight against age-related diseases. Obesity, the authors write, speeds up the aging of the immune system by targeting different immune cells, and that later weight reduction will not always reverse the process.

The effects of obesity on the immune system, in turn, affect susceptibility to diseases like influenza, which often affects patients with obesity at a higher rate than normal-weight individuals. Obese people are also at higher risk of sarcopenia, a disease usually associated with aging that features a progressive decline in muscle mass and strength.

Finally, the paper emphasizes how individuals with obesity are more susceptible to diseases closely associated with later-life onset, such as type 2 diabetes, Alzheimer’s and various forms of cancer.

Santosa says the inspiration for this study came to her when she saw how many obese kids were developing adult-onset conditions of diseases, such as hypertension, high cholesterol and type 2 diabetes. She also realized that the comorbidities of obesity were similar to that of aging.

“I ask people to list as many comorbidities of obesity as they can,” Santosa said. “Then I ask how many of those comorbidities are associated with aging. Most people will say, all of them. There is certainly something that is happening in obesity that is accelerating our aging process.”

Source: Concordia University

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[gravityresearch]

Jean-Martin Charcot's careful clinical and pathological account of a patient with demyelinating lesions or “sclérose en plaques” in 1868 provided the world with the first clear description of multiple sclerosis (MS) [1]. Despite almost a century and a half of our acquaintance with this disease, its pathogenesis remains elusive and we continue to lack therapeutic options to treat progressive MS [2].

Eighty-five per cent of cases of MS present with recurring episodes of isolated neurological syndromes, which usually resolve with conservative management (termed relapsing and remitting or RRMS). The remaining 15% of cases present with a gradual and progressive loss of neurological function that does not recover (termed primary progressive or PPMS). Of the 85% of the cases who present with RRMS, the majority begins to suffer from progressive neurological decline after one to three decades (termed secondary progressive or SPMS) that is similar in pattern to PPMS [3, 4].

MS has traditionally been viewed as an immune-mediated inflammatory disease. An immune response is thought to be responsible for causing the spontaneously remitting relapses in RRMS. Immune cells migrate across a compromised blood brain barrier and cause the focal and disseminated inflammation typical for RRMS. The traditional view of MS as an inflammatory disease has resulted in almost all therapeutic strategies taking an immunomodulatory or immunosuppressive approach [2].

The idea of MS having a primarily inflammatory component is challenged by the observation that focal inflammation may be absent in a minority of cases of progressive MS [5]. Neurodegeneration may play a more central role in its pathogenesis [6]. As the majority of current therapeutic options for MS are based on immune therapy, there is at present no definitive therapy for progressive MS, whether primary or secondary [7].

Accumulating evidence of a dissociation between inflammation and disease progression warrants a revised perspective on the role of neurodegeneration in the pathogenesis of MS and therefore the therapeutic strategies. In this review, we explore the evidence of neurodegeneration and the players in its pathogenesis that lead us to the potential of the ketogenic diet for use as a therapy for progressive MS.

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2. Is MS Primarily a Neurodegenerative Disease?

The traditional model of MS is based on an “outside-in” approach. In this model, a dysregulated immune system attacks the central nervous system. Peripheral immune cells cross a compromised blood brain barrier to enter the central nervous system and give rise to acute multifocal inflammatory lesions, which are either asymptomatic or manifest as relapses in RRMS involving a variety of neurological symptoms disseminated in time. Although RRMS is the commonest mode of MS presentation, the vast majority of patients presenting in this way enter into a progressive phase of MS (SPMS) as long as three decades after disease onset.

The duality of the inflammatory and neurodegenerative components is made salient by the observation that MS can “worsen” at exactly the same rate regardless of whether a patient started off with decades of isolated inflammatory relapses or entered directly into progressive MS. Pathophysiologically, no difference can be found between the two disease phenotypes [8, 9].

2.1. An Alternative Model of MS

Such evidence of a distinct dissociation between disease progression and inflammation has challenged the traditional “outside-in” approach. Progression in the absence of immune attacks is indicative of a separate and parallel pathogenic process. Some authors have proposed an “inside-out” model of MS where primary cellular degeneration is the initiating factor that then triggers inflammation [10]. The degeneration releases antigenic cellular matter that then invites an immune response.

2.2. Halting Inflammation Does Not Halt Disease Progression

Although there is as yet no conclusive evidence to suggest that degeneration might be the initial event that triggers the inflammation seen in MS (the age-old chicken and egg question), clinical findings support a dissociation between the two, where, at the very least, degeneration does not follow inflammation and may occur independently of inflammation. Most varieties of immune-modulating therapy that reduce and even eliminate inflammation have little bearing on the progress of MS in the very long-term, although a few of the newer immunomodulatory agents may hold greater promise [11–14]. Autologous haematopoietic stem cell transplantation therapy, though highly efficacious at reducing inflammation, does not halt axonal degeneration and brain atrophy [15]. Progressive neurodegeneration and axonal atrophy in the absence of inflammation are observed in MS [16].

2.3. Harding Syndrome

There is pathological evidence in support of the theory that neurodegeneration may occur in complete isolation in MS without any evidence of preceding inflammation: foci of damage have been observed in the inner layers of the myelin sheath with the outer layers remaining intact. This starkly challenges the possibility of a T cell mediated external mechanism [17, 18]. In Harding syndrome, there is evidence that neurodegeneration precedes and then causes the neuroinflammation seen in classical MS. In this condition, the cellular degeneration occurring as a result of defective mitochondrial function may trigger an autoimmune response in those who are “immunologically primed” [19]. Although Leber Hereditary Optic Neuropathy (LHON) is more penetrant in males, females are at greater risk of autoimmune disease and this may explain why there is a higher incidence of Harding syndrome with MS-like inflammation in females, despite involving the same mutation as LHON [20].

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3. The Role of Mitochondria in Multiple Sclerosis

Whether neurodegeneration triggers inflammation or is triggered by inflammation or occurs as a parallel process, the evidence that MS involves neurodegeneration as well as neuroinflammation is ever increasing. Mitochondrial dysfunction is thought to play a central role in the neurodegenerative disease process and a growing body of evidence suggests that mitochondrial dysfunction may also be of great importance in the pathogenesis of MS [21, 22].

3.1. Mitochondrial Function May Determine the Fate of “Struggling” Axons

Axonal degeneration is a prominent feature of MS and is notably present even in the absence of local demyelination [23, 24]. Animal models suggest that mitochondrial injury may be a necessary step preceding axonal degeneration. The generation of reactive oxygen species may contribute to mitochondrial injury as the detoxification of reactive oxygen species reverses the injury and halts axonal degeneration [25].

Once chronically demyelinated, some axons degenerate while others may survive. It seems possible that mitochondrial “stealth” may determine the fate of demyelinated axons. Degenerating axons are seen to contain dysfunctional mitochondria, whereas the axons that survive demyelination contain highly functional mitochondria with increased respiratory chain activity [26, 27]. These findings mirror a recent study on glaucomatous optic neuropathy where it was observed that robust mitochondria may offer protection from neurodegeneration despite the presence of high intraocular pressures [28]. It is thought that, where axons degenerate following demyelination, they do so when energy production by mitochondria becomes inadequate. Mitochondrial function seems to determine the fate of axons under duress.

3.2. Mitochondrial Dysfunction Is Seen in “Normal Appearing” Grey Matter

Grey matter atrophy is a recognized feature of MS and the rate of atrophy is seen to increase as the RRMS stage progresses to SPMS [29]. Furthermore, neuronal atrophy can be seen to occur independently of demyelination, in areas of “normal appearing grey matter” as ascertained by immunohistochemical staining techniques and microscopy [30]. Mitochondrial function within cortical neurons in MS has been shown to be compromised. Campbell et al. (2011) used complex IV/complex II histochemistry, immunohistochemistry, laser dissection microscopy, and PCR and DNA sequencing methods to demonstrate a striking reduction in the activity of complexes II and IV within the oxidative phosphorylation chain in neurons obtained from autopsies of cases of SPMS [31].

3.3. Progressive Mitochondrial Compromise May Correlate with Reduced Recovery from Relapses

Levels of the transcriptional cofactor PGC-1a, which plays a key role in the activation of nuclear transcription factors involved in mitochondrial function, may be reduced in cortical neurons in progressive MS. Its expression was found to correlate with neuronal density [32]. Given the observation that the rate of brain atrophy increases as RRMS progresses to the SPMS, the decline in PGC-1a may suggest a parallel worsening in mitochondrial function [33]. During this stage of progression, recovery from relapses becomes progressively incomplete [34]. The progressive decline in mitochondrial function with a resulting decrease in ATP availability may plausibly cause a decline in axonal resilience, making recovery from each episode of relapse increasingly difficult.

A reduction in PGC-1a levels has also been observed in other neurodegenerative conditions such as Alzheimer disease [35].

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4. Mitochondria and Neurodegeneration

Several groups have proposed a model for neurodegeneration in which mitochondrial dysfunction is central to its pathogenesis [36, 37]. In this model, mitochondrial dysfunction precedes synaptic dysfunction, atrophy, and neuronal loss.

In an animal model of MS, experimental autoimmune encephalomyelitis (EAE), mitochondrial injury has been shown to precede inflammation and to be the trigger for neurodegeneration [38]. Although the precise molecular pathways leading to mitochondrial damage remain unknown, oxidative damage is one possible route [39].

Early studies of antioxidant therapies in animal models of MS are showing promising results. Superoxide dismutase 2 has been shown to salvage axonal loss in EAE-related optic neuritis [40]. A synthetic antioxidant, Mito-Q, has been shown to be neuroprotective and delay disease progression in EAE, despite having no effect on inflammation, further confirming a dissociation between the two disease processes and demonstrating that neurodegeneration might be more worthy of therapeutic intervention in order to improve disease prognosis [41].

To date, one of the few available therapeutic options used in MS that may have some beneficial effects on progressive MS is Dimethyl Fumarate or DMF [42]. DMF is the only current therapy for MS that in addition to having an immunomodulatory effect is also a potent antioxidant agent. It is thought to reduce oxidative stress through the NRF-2 pathway and hence have a neuroprotective effect [43]. This neuroprotective effect has also been evident in other neurodegenerative settings [44].

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5. Mitochondria as the Therapeutic Target for Progressive MS

The paucity of treatment options for progressive MS indicates an urgent need to find therapeutic targets. The role of mitochondrial dysfunction in neurodegeneration suggests that targeting mitochondrial function may be a useful therapeutic strategy for progressive MS although clinical trials examining the efficacy of agents promoting mitochondrial function in non-MS diseases with known mitochondrial pathology have shown variable results. Some of this variability may stem from differences and difficulties faced with drug delivery and dosage [45].

There are a limited number of studies to date testing the efficacy of agents that target mitochondrial function in the setting of MS, but they offer considerable promise in the efficacy of mitochondria-targeted therapy. Coenzyme Q10 has antioxidant properties and forms part of the electron transport chain interacting with complex I. A randomized placebo-controlled double-blind study of Coenzyme Q10 supplementation over 12 weeks in patients with relapsing and remitting MS demonstrated a reduction in IL-6 and MMP-9 levels [46]. The results of another similar trial by the same group demonstrated a reduction in depression and fatigue [47].

Mouse models of MS (EAE) are based on an immune/inflammatory model and not a degenerative model limiting the ability of the mouse model to accurately reflect the oxidative damage occurring in human MS. This may explain some inconsistencies in the results obtained from mouse model studies of MS [48, 49]. Mito-Q, an antioxidant that contains ubiquinone, has been shown to delay disease progression and reduce neuronal cell loss in a mouse model of multiple sclerosis; however, one study using a synthetic analogue of Coenzyme Q10 failed to prevent disease progression [50].

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6. Glucose Hypometabolism

Some studies have suggested that there may be a bioenergetic shift taking place within neuronal metabolism prior to the onset of clinical signs of neurodegeneration, where glucose uptake and utilization become progressively reduced. This glucose hypometabolism may reflect a decline in mitochondrial function. The shift has been observed to occur long before the onset of clinical signs of neurodegeneration, suggesting the possibility that glucose hypometabolism may be the initial step leading to axonal atrophy and neuronal loss through a reduction in ATP availability [51–54]. The bioenergetic shift appears to specifically affect the metabolism of glucose. No such shift is seen with ketone body metabolism [54, 55].

6.1. Glucose Hypometabolism in MS

The neurodegenerative process underlying progressive MS may also result in glucose hypometabolism. This would suggest a potential therapeutic advantage in boosting energy supply through an alternative route, such as ketone metabolism. A study that compared 47 MS patients with varying levels of fatigue and 16 healthy controls showed that the patients had reduced cerebral glucose metabolism in various regions within the brain, including the prefrontal, premotor, and supplementary motor areas and the putamen when compared to control subjects. There was an inverse correlation between degree of fatigue and glucose metabolic rate [56]. Another study on 8 MS patients and 8 gender matched healthy control subjects demonstrated lower glucose uptake in 40% of the brain compared to healthy controls [57].

Extramitochondrial metabolism increases in the presence of impaired mitochondrial metabolism of glucose. In a pilot study comparing 85 patients with relapsing and remitting MS and 54 patients with secondary progressive MS as well as 18 healthy controls, extramitochondrial glucose metabolism showed a correlation with disease progression, suggesting that impaired mitochondrial metabolism of glucose may play a significant role in disease progression in progressive MS [58].

Further molecular evidence of impaired glucose metabolism playing a role in MS is seen in the altered distribution of glucose (GLUT) and monocarboxylate transporters (MCT) within chronic lesions of MS where there is a decline in axonal GLUT3 and MCT2 expression. These changes may confer resistance to glucose entry into demyelinated axons, depriving them of adequate fuel supply resulting in glucose hypometabolism [59].

The possibility that providing the brain with an alternative source of fuel may reduce the rate of neurodegeneration is a promising avenue to explore, particularly where there remains a paucity of therapeutic options [60].

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7. The Potential of Ketones to Provide an Alternative Fuel Supply

In 1967, Cahill et al. demonstrated that, during prolonged fasting, the body provides the brain with an alternative source of fuel, in the form of ketone bodies. The central nervous system is unable to use fat as a direct energy source and after prolonged carbohydrate restriction, fat is converted into ketone bodies in a process referred to as “ketogenesis.” Ketogenesis takes place primarily within the matrix of mitochondria located within the liver. Ketogenesis results in the production of the ketone bodies beta-hydroxybutyrate, acetoacetate, and acetone which replace glucose as the brain's main sources of fuel [61]. Hans Krebs first made the distinction between the normal, “physiological” ketosis that is induced when following a carbohydrate-restricted diet where levels of ketones do not exceed 8 mmol/L and diabetic ketoacidosis, a complication of diabetes where ketonaemia can exceed 20 mmol/L and result in acidosis [62]. Ketone bodies can easily cross the blood brain barrier and the brain's usage of ketone bodies increases as their concentration in the serum increases, up to a concentration of 12 mmol/L [63]. A meta-analysis of animal studies has shown that the cerebral metabolic rate of glucose decreases 9% with every 1 mmol/L increase in total plasma ketones. Ketones bypass the glycolytic pathway and directly enter the Tricarboxylic Acid (TCA) cycle within mitochondria, contributing to anaplerosis.

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8. A Ketogenic Diet for the Neurodegenerative Component of Progressive MS

The ketogenic diet has traditionally been used for the treatment of resistant epilepsy, but it is increasingly becoming apparent that its benefits may apply to a wider spectrum of neurological disease. Although research on its use outside the realms of epilepsy is still at its infancy, the findings are promising and hold great potential for the treatment of neurodegeneration, particularly with regard to mitochondrial function.

A ketogenic diet has a favourable effect on mitochondrial function. It reduces levels of reactive oxygen species and increases ATP availability. The diet may provide neuroprotection and reduce inflammation. Ketones produced during a ketogenic diet can be used as an alternative source of fuel in the setting of impaired glucose metabolism.

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9. The Effect of the Ketogenic Diet on Oxidative Stress

A ketogenic diet has been shown to reduce the generation of reactive oxygen species through its effect on uncoupling proteins. It also increases levels of antioxidant agents including catalase and glutathione through its inhibitory action on histone deacetylases and activation of the Nrf2 pathway.

9.1. The Ketogenic Diet Increases Mitochondrial Uncoupling Protein Levels

The process of oxidative phosphorylation generates reactive oxygen species. The extent of reactive oxygen species generation correlates strongly with the potential difference across the inner mitochondrial membrane. Uncoupling proteins (UCPs) can reduce this potential difference by allowing the entry of protons into the mitochondrial matrix. Although this “mild” uncoupling may incur a small reduction in ATP generated through oxidative phosphorylation, its overall net effect is to enhance respiration and ATP levels through a reduction in reactive oxygen species formation and protection from apoptotic events [64]. A ketogenic diet appears to promote UCP activity, specifically the activity of UCP2, UCP4, and UCP5 with a corresponding decline in reactive oxygen species [65].

9.2. Ketones Inhibit Histone Deacetylases

The ketone beta-hydroxybutyrate has a direct, dose-dependent inhibitory activity on class I histone deacetylases (HDACs) including HDAC1, HDAC3, and HDAC4. The ketone acetoacetate has also been shown to inhibit class I and class IIa HDACs. Beta-hydroxybutyrate's inhibition of HDAC promotes the acetylation of histone H3 lysine 9 and histone H3 lysine 14 and increases the transcription of genes regulated by FOXO3A. These include genes leading to the expression of the antioxidant enzymes mitochondrial superoxide dismutase and catalase [66].

9.3. A Ketogenic Diet Leads to the Activation of the Nrf2 Pathway

The ketogenic diet raises glutathione levels in the hippocampus of rats [67]. This is thought to occur through the Nrf2 (nuclear factor erythroid 2-related factor) pathway. When the ketogenic diet is first initiated, there is a temporary increase in oxidative stress. This may be activating Nrf2, since, a week after the temporary rise in oxidative stress, there is increased expression of Nrf2. Three weeks after the start of the diet, oxidative stress declines to below baseline levels and Nrf2 remains raised [68].

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10. The Effect of the Ketogenic Diet on ATP Levels

A ketogenic diet enhances ATP production. The administration of beta-hydroxybutyrate immediately following bilateral common carotid artery ligation in a mouse model of global cerebral ischaemia preserves ATP levels [69]. Feeding mice a ketogenic diet for three weeks resulted in increased levels of ATP and the ATP/ADP ratio in the brain [70].

The improvement in ATP levels may partly be explained through the ability of the ketogenic diet to reduce oxidative stress. Although the diet may reduce reactive oxygen species generation through an increase in UCP activity, any reduction in oxidative phosphorylation incurred through UCP activity is outweighed by the enhancement of respiration and associated ATP production occurring as a result of reduced oxidative stress.

A ketogenic diet also appears to preserve ATP levels in the event of mitochondrial respiratory chain dysfunction, possibly through the replenishment of TCA cycle intermediates [71]. Beta-hydroxybutyrate attenuates the decrease in ATP production caused by a defect in complex I of the electron transport chain. It is thought to increase levels of the TCA intermediate succinate, which bypasses complex I when entering the TCA cycle [65, 72]. This carries considerable implications for MS, since defects in complex I within the electron transport chain have been observed in white matter lesions as well as in “normal” regions of the motor cortex [39, 73]. Ketones can also preserve ATP levels if complex II of the electron transport chain is inhibited, but this effect shows some regional specificity [74].

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11. The Effect of the Ketogenic Diet on Mitochondrial Biogenesis

Mitochondrial biogenesis within the rat hippocampus and cerebellar vermis is increased by the ketogenic diet [75, 76]. Although the precise pathway for this is not known, it is thought to involve the PGC1α family of transcriptional coactivators, which promote transcription factors including NRF-1, NRF-2, and ERRα[77].

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12. The Effect of the Ketogenic Diet on Inflammation

The anti-inflammatory effect of a ketogenic diet has been demonstrated in a murine model of lipopolysaccharide-induced fever [78]. In a rat model of MS, the diet suppressed the expression of inflammatory cytokines and enhanced CA1 hippocampal synaptic plasticity and long-term potentiation, which resulted in improved learning, memory, and motor ability [79]. The anti-inflammatory effect of a ketogenic diet may partly be explained through the inhibition of the NLRP3 inflammasome by beta-hydroxybutyrate in a manner that is independent of starvation-induced mechanisms such as AMPK, autophagy, or glycolytic inhibition. The NLRP3 inflammasome is responsible for the cleavage of procaspase-1 into caspase-1 and the activation of the cytokines IL-1β and IL-18. Its inhibition prevents IL-1β and IL-18 generation and their downstream effects [80].