Warning: Angst. @suchabigmesss asked me to pick up her heart from the floor, just an indicator.
A/N: Hi loves! It’s finally here, so sorry for the delay! Definitely do read part 1 first!! Thank you so incredibly much for all the love you give me and this story! This will be a multichapter series, so I really hope you’ll want to read it, I have an outline ready and chapters will be out faster than this one! I promise! Lots of love to all of your cute faces! feedback is as always greatly appreciated <3
Bucky looked at the hologram in front of him, gritting his teeth in annoyance. He had raided every Hydra base he could think of and more, but not as much as a stray of hair of evidence had been found of your whereabouts. His eyes scanned the map again, his brain working overtime to think of something he hadn’t thought of, something he couldn’t remember. Just something.
He came up with nothing.
Groaning in frustration, he dismissed the hologram and fell back in the chair. He stared out of the window at the night sky being lit up by a few stars, letting his mind run wild.
Seven months and twenty four days. That’s how long it had been since you had sacrificed yourself, going with Hydra so they wouldn’t hurt him or Natasha.
Whenever he closed his eyes, all he could see was the last look you gave him. A silent plea for him to step over the line so they would kill you instead of taking you with them. He hadn’t listened to your plea because he couldn’t stand letting you die. He had done what he wanted, let you live, and because of that, you were God knows where among the people who had ripped him from everything he was and made him into something they wished.
I just want a drunk Stiles to just turn to Derek at Jungle and be like, “Dude, I knew I loved you when you tried to order me off your property. You were like the forbidden fruit after that. I just wanted to lick, to taste; to just sink my teeth into you.” Derek slowly turns towards him with both eyebrows flying so high off his forehead he’d need clearance from the government to continue. He just looks Stiles up and down before turning back, “I know ” - the ‘ditto’ going unspoken but known all the same. Stiles practically falls off his bar stool because, “Dude, did you just Han Solo me?! That’s so fuckin’ hot.” Derek just smirks into his beer as he takes a leisurely sip with hopes and dreams of what’s finally to come.
Joshua Buckholtz wants to change the way you think about psychopaths — and he’s willing to go to prison to do it.
An associate professor of psychology at Harvard, Buckholtz is the senior author of a study that relies on brain scans of nearly 50 prison inmates to help explain why psychopaths make poor decisions that often lead to violence or other anti-social behavior.
What they found, he said, is that psychopaths’ brains are wired in a way that leads them to overvalue immediate rewards and neglect the future consequences of potentially dangerous or immoral actions. The study is described in a July 5 paper in Neuron.
“For years, we have been focused on the idea that psychopaths are people who cannot generate emotion and that’s why they do all these terrible things,” Buckholtz said. “But what we care about with psychopaths is not the feelings they have or don’t have, it’s the choices they make. Psychopaths commit an astonishing amount of crime, and this crime is both devastating to victims and astronomically costly to society as a whole.”
“And even though psychopaths are often portrayed as cold-blooded, almost alien predators, we have been showing that their emotional deficits may not actually be the primary driver of these bad choices. Because it’s the choices of psychopaths that cause so much trouble, we’ve been trying to understand what goes on in their brains when they make decisions that involve trade-offs between the costs and benefits of action,” he continued. “In this most recent paper … we are able to look at brain-based measures of reward and value and the communication between different brain regions that are involved in decision-making.”
Obtaining the scans used in the study, however, was no easy feat — where most studies face an uphill battle in bringing subjects into the lab, Buckholtz’s challenge was in bringing the scanner to his subjects.
The solution came in form of a “mobile” scanner transported in a tractor-trailer. The scanner is typically used for cancer screenings in rural areas. After trucking the equipment to two medium-security prisons in Wisconsin, the team, which included collaborators at the University of Wisconsin, Madison, and the University of New Mexico, would spend days calibrating the scanner, and then work to scan as many volunteers as possible as quickly as possible.
“It was a huge undertaking,” he said. “Most MRI scanners, they’re not going anywhere, but in this case, we’re driving this inside a prison and then in very quick succession we have to assess and scan the inmates.”
The team ultimately scanned the brains of 49 inmates over two hours as they took part in a delayed gratification test that asked them to choose between two options: receive a smaller amount of money immediately, or a larger amount at a later time. The results of the tests were then fit to a model that allowed researchers not only to measure how impulsive each participant’s behavior was, but to identify brain regions that played a role in assessing the relative value of such choices.
What they found, Buckholtz said, was people who scored high for psychopathy showed greater activity in a region called the ventral striatum — known to be involved in evaluating the subjective reward — for the more immediate choice.
“So the more psychopathic a person is, the greater the magnitude of that striatal response,” Buckholtz said. “That suggests that the way they are calculating the value rewards is dysregulated — they may overrepresent the value of immediate reward.”
When Buckholtz and colleagues began mapping which brain regions were connected to the ventral striatum, it became clear why.
“We mapped the connections between the ventral striatum and other regions known to be involved in decision-making, specifically regions of the prefrontal cortex known to regulate striatal response,” he said. “When we did that, we found that connections between the striatum and the ventral medial prefrontal cortex were much weaker in people with psychopathy.
That lack of connection is important, Buckholtz said, because this portion of the prefrontal cortex is thought to be important for “mental time-travel” — envisioning the future consequences of actions. There is increasing evidence that the prefrontal cortex uses the outcome of this process to change how strongly the striatum responds to rewards. With that prefrontal modulating influence weakened, the value of the more immediate choice may become dramatically overrepresented.
“The striatum assigns values to different actions without much temporal context,” he said. “We need the prefrontal cortex to make prospective judgements how an action will affect us in the future — ‘If I do this, then this bad thing will happen.’ The way we think of it is if you break that connection in anyone, they’re going to start making bad choices because they won’t have the information that would otherwise guide their decision-making to more adaptive ends.”
The effect was so pronounced, Buckholtz said, that researchers were able to use the degree of connection between the striatum and the prefrontal cortex to accurately predict how many times inmates had been convicted of crimes.
Ultimately, Buckholtz said, his goal is to erase the popular image of psychopaths as incomprehensible, cold-blooded monsters and see them for what they are — human beings whose brains are simply wired differently.
“They’re not aliens, they’re people who make bad decisions,” he said. “The same kind of short-sighted, impulsive decision-making that we see in psychopathic individuals has also been noted in compulsive overeaters and substance abusers. If we can put this back into the domain of rigorous scientific analysis, we can see psychopaths aren’t inhuman, they’re exactly what you would expect from humans who have this particular kind of brain wiring dysfunction.”
Friend who doesn’t know anything about musicals: musical theatre must be so fun! All they do sing and dance all the time! And the music is so upbeat, is that why you like it? Because it makes you smile?
Me *looking at them through tears while thinking about “falsettos”, “the last five years”, “dear Evan Hansen”, “fun home"*: yeah…. totally
A landmark project to map the wiring of the human brain from womb to
birth has released thousands of images that will help scientists unravel
how conditions such as autism, cerebral palsy and attention deficit
disorders arise in the brain.
The first tranche of images come from 40 newborn babies who were
scanned in their sleep to produce stunning high-resolution pictures of
early brain anatomy and the intricate neural wiring that ferries some of
the earliest signals around the organ.
The initial batch of brain scans are intended to give researchers a
first chance to analyse the data and provide feedback to the senior
scientists at King’s College London, Oxford University and Imperial
College London who are leading the Developing Human Connectome Project,
which is funded by €15m (£12.5m) from the EU.
Diffusion MRI showing connections in the developing brain.
Photograph: The Developing Human Connectome Project
The images show the intricate neural wiring that ferries some of the earliest signals around the brain.
Photograph: The Developing Human Connectome Project
3D reconstruction of the cortical surface and calculated features from a
seven-month, eight-month and nine-month baby brain MRI. From top to
bottom: white matter surface, cortical surface, inflated surface,
parcellation into different structures, sulcal depth maps, mean
curvature, cortical thickness and T1/T2 myelin maps. Photograph: The
Developing Human Connectome Project
Body dysmorphia isn’t a problem with what the brain expects of the body (the way transsexualism and BIID both appear to be), it’s a problem with one’s perception of the body. That might sound like the same thing, but it’s not.
A pre-transition transgender woman looks in the mirror and sees a male body. Her perception is correct; it is in fact a male body. The reality of her male body is what pains her. Her brain expects a female body. It doesn’t ‘recognize’ her male parts.
A thin anorexic girl looks in the mirror and sees a fat body. Her perception is wrong; she is already thin, but still believes she needs to lose weight. This is how body dysmorphia works. She sees a huge nose, when she has a very small one. She sees breasts that are far too small, when she’s already gone through three boob jobs to go through cup sizes D, E and F.
The transgender person’s problem is with the actual body.
The body dysmorphic person’s problem is between the ears.
It has nothing to do with the brain’s “expectation”, because while the brain is sexually dimorphic and the brain-body map expects certain body parts, this has no connection with weight or other specific details. There is no problem with ‘connection’ between the brain and the body here. The problem is a psychological one; perfectionism, trauma,
extreme self-esteem issues, which latches onto the body and ends up expressed through body dysmorphia.
Which is why they can change and change and it will never be enough. Because the feelings underneath, the actual root of the problem, aren’t affected by surgery. They can only be treated with therapy.
The Genes and Neural Circuits Behind Autism’s Impaired Sociability
Researchers at Beth Israel Deaconess Medical Center (BIDMC) have gained
new insight into the genetic and neuronal circuit mechanisms that may
contribute to impaired sociability in some forms of Autism Spectrum
Disorder. Led by Matthew P. Anderson,
MD, PhD, Director of Neuropathology at BIDMC, the scientists determined
how a gene linked to one common form of autism works in a specific
population of brain cells to impair sociability. The research, published
in the journal Nature, reveals the neurobiological control of
sociability and could represent important first steps toward
interventions for patients with autism.
Anderson and colleagues focused on the gene UBE3A, multiple copies of
which causes a form of autism in humans (called isodicentric chromosome
15q). Conversely, the lack of this same gene in
humans leads to a developmental disorder called Angelman’s syndrome,
characterized by increased sociability. In previous work, Anderson’s
team demonstrated that mice engineered with extra copies of the UBE3A
gene show impaired sociability, as well as heightened repetitive
self-grooming and reduced vocalizations with other mice.
“In this study, we wanted to determine where in the brain this social
behavior deficit arises and where and how increases of the UBE3A gene
repress it,” said Anderson, who is also an Associate Professor in the
Program in Neuroscience at Harvard Medical School and Director of Autism
BrainNET Boston Node. “We had tools in hand that we built ourselves. We
not only introduced the gene into specific brain regions of the mouse,
but we could also direct it to specific cell types to test which ones
played a role in regulating sociability.”
When Anderson and colleagues compared the brains of the mice
engineered to model autism to those of normal – or wild type (WT) –
mice, they observed that the increased UBE3A gene copies interacted with
nearly 600 other genes. After analyzing and comparing protein
interactions between the UBE3A regulated gene and genes altered in human
autism, the researchers noticed that increased doses of UBE3A repressed
Cerebellin is a family of genes that physically interact with other
autism genes to form glutamatergic synapses, the junctions where neurons
communicate with each other via the neurotransmitter glutamate. The
researchers chose to focus on one of them, Cerebellin 1 (CBLN1), as the
potential mediator of UBE3A’s effects. When they deleted CBLN1 in
glutamate neurons, they recreated the same impaired sociability produced
by increased UBE3A.
“Selecting Cerebellin 1 out of hundreds of other potential targets was
something of a leap of faith,” Anderson said. “When we deleted the gene
and were able to reconstitute the social deficits, that was the moment
we realized we’d hit the right target. Cerebellin 1 was the gene
repressed by UBE3A that seemed to mediate its effects.”
In another series of experiments, Anderson and colleagues
demonstrated an even more definitive link between UBE3A and CBLN1.
Seizures are a common symptom among people with autism including this
genetic form. Seizures themselves when sufficiently severe, also
impaired sociability. Anderson’s team suspected this seizure-induced
impairment of sociability was the result of repressing the Cerebellin
genes. Indeed, the researchers found that deleting UBE3A, upstream from
Cerebellin genes, prevented the seizure-induced social impairments and
blocked seizures ability to repress CBLN1.
“If you take away UBE3A, seizures can’t repress sociability or
Cerebellin,” said Anderson. “The flip side is, if you have just a little
extra UBE3A – as a subset of people with autism do – and you combine
that with less severe seizures - you can get a full-blown loss of social
The researchers next conducted a variety of brain mapping experiments
to locate where in the brain these crucial seizure-gene interactions
“We mapped this seat of sociability to a surprising location,“
Anderson explained. Most scientists would have thought they take place
in the cortex – the area of the brain where sensory processing and motor
commands take place – but, in fact, these interactions take place in
the brain stem, in the reward system.”
Then the researchers used their engineered mouse model to confirm the
precise location, the ventral tegmental area (VTA), part of the
midbrain that plays a role in the reward system and addiction. Anderson
and colleagues used chemogenetics – an approach that makes use of
modified receptors introduced into neurons that responds to drugs, but
not to naturally-occurring neurotransmitters – to switch this specific
group of neurons on or off. Turning these neurons on could magnify
sociability and rescue seizure and UBE3A-induced sociability deficits.
“We were able to abolish sociability by inhibiting these neurons and
we could magnify and prolong sociability by turning them on,” said
Anderson. “So we have a toggle switch for sociability. It has a
therapeutic flavor; someday, we might be able to translate this into a
treatment that will helps patients.”
Scientists Become Research Subjects in After-Hours Brain-Scanning Project
A quest to analyze the unique features of individual human brains evolved into the so-called Midnight Scan Club, a group of scientists who had big ideas but almost no funding and little time to research the trillions of neural connections that activate the body’s most powerful organ.